Seminal Fluid And Effects Of Metals On It Biology Essay

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Seminal fluid is a substance found in many male species sexual reproductive glands. Semen is the cloudy white body fluid that is emitted from the urethra of the penis during ejaculation. It is made up of a variety of molecules and cells such as leucocytes, proteolytic and other enzymes as well as fructose and is a medium for excretion and transportation of spermatozoa. In the human male species, production occurs in the prostate glands and gonadal which are somewhat unappreciated sex accessory glands until they malfunction or cease to function at all with the prevailing effects being drastically lower the rates of fertility.

Semen is composed mostly of water, probably about 90% by weight. After that, it's a mixture of amino acids (proteins), minerals, carbohydrates (sugars), and a small number of other things. Semen has a basic pH level meaning it is the opposite of acidic by nature - this is to counteract and neutralize the vagina's acidic pH and increase the spermatozoa's chances of survival.

Source:(http://www.orgasmpower.net/semen-production.html)

Besides sperm, semen is made of secretions from the seven lower urinary tract structures. These structures include: seminal vesicles (which account for 60-70% of the fluid), prostate gland (which accounts for 20-30%) and the remaining percentage is shared by the epididymis, vas deferens, ampullae of the vas, Cowper's glands and glands of Littre. Semen itself has high concentrations of potassium, zinc, citric acid, fructose, phosphorylcholine, spermine, free amino acids, prostaglandins and enzymes, which nourish and protect the sperm. Source:(http://www.menstuff.org/issues/byissue/semen.html#funfacts)

Source : http://www.proceptin.com/phc/sperm-cell.php

Main Production sites 

Seminal fluid is mostly produced in four places; in the seminal vesicles, the male testes, the prostate gland and in the Cowper's glands.

The Seminal Vesicles: This is where the milky white protein based substance (semenogelin I and II) that semen mostly consists of is mainly produced (Ulvsback et al. 1992). These semenogelins interact with each other and coagulumate after ejaculation (Aumuller and Riva 1992). (Spermatozoa health depends on this substance for nutrients which they will use to sustain them on their way to fertilize the female ova.  This fluid is also alkaline in nature and helps to neutralize the acidic conditions within the female reproductive system.

The Male Testes: This is the organ where the production of sperm cells occurs. Spermatozoa cells are cultivated here until they mature. After that they are then stored in the Ampulla where they wait to be ejaculated out of the body. They are also protected by glycocalyx secretions from the testis, efferent ducts, epididymis and accessory glands (Schroeter et al. 1999).

The Prostate Gland: The prostate gland also produces an alkaline solution that acts as a protective barrier for the sperm cells against the acidity of the female sexual reproductive environment. The pH of the fluid is maintained above 7 by the action of prostatic prostasomes (et al. 1999). The fluid produced, is a protastic serine protease and helps the liquification of the semenogelins coagulum (Peter et al. 1998) The prostate is also an important source of superoxide anion collectors in humans (Gavella et al. 1996)

 The Cowper's Glands: These glands produce a clear slippery liquid also known as pre-cum which is excreted during foreplay or sexual stimulation. It is produced by the Cowper's or bulbouretheral glands and creates a medium for which sperm can be transported and swim in through the male reproductive tract and acts as a lubricant to reduce friction during sexual activity.

Seminal fluid Composition and functions

Semen contains citric acid, free amino acids, fructose, enzymes, phosphorylcholine, prostaglandin, potassium, and zinc. The average volume of semen produced in a single ejaculation varies from 2 to 5 ml. The semen from a single ejaculation may contain between 40 million and 600 million sperm, depending on the volume of the ejaculate and the length of time since the last ejaculation. Samples used for medical purposes are obtained by having the donor masturbate. If a sample cannot be produced without sexual intercourse, non-reactive condoms can be used to collect the semen.

The process of secretion of seminal fluid in male mammals is ultimately under androgenic and estrogenic control, with a compounding effect occurring between these two types of gonadal steroids (Reaside et al. 1999). Oxytocin secreted by the posterior pituitary, prolactin secreted by the anterior can also control activity of sexual accessory glands in mammals (Gemmell and Sernia 1989; Kumar and Farooq 1994; Gonzalez et al. 1994; Watson et al. 1999).

There is a general consensus that the three major functional aspects of seminal fluid are, its role in sperm competition, its function to aid fertility and lastly its role in the transmission of venereal diseases. This is due to the composition of the seminal fluid being attributed to the secretion of many different tissues and that are under the control of a variety of different components of the neuroendocrine system. The functionality of the seminal fluid components may be duplicated but in the process they will synergize and complement each other. As an example, increased immunosuppressive action of the seminal fluid on the female reproductive tract aimed at increasing sperm viability may also facilitate the transmission of sexually transmissible pathogens, thus increasing the selection pressure on females to overcome immunosuppression. (Birkhead et al. 1993).

Seminal fluid is responsible for sperm capacitation for the ability to fertilize female's ova. Also some proteins secreted by male accessory glands have been implicated in the process of sperm capacitation. (Gillott 1996). Structural proteins of the spermatophre that are secreted by sex accessory glands, such as trehalase and sugars such as trehalose, may play a role in the activation of sperm within the female's bursa copulatrix (Yaginuma et al. 1996). The process of capacitation of sperm involves the acquisition of a coat of carbohydrates that from the glycocalyx (Schroeter et al. 1999). Most of those carbohydrates are attached to proteins forming glycoprotein complexes that are produced by accessory glands and other tissues of the male reproductive system. Acquisition of a glycocalyx is essential in some taxa for the attainment of full capacitation of sperm and fertilizing ability .(Schroeter et al.1999).

In men, accessory glands secrete 5'-necleotidase, an enzyme that hydrolyses nuleotides into phosphate and nucleosides, which may play a role in the modification of sperm surface during capacitation (Konrad et al. 1998). Capacitation in human sperm is also increased by tripeptide amides found in seminal plasma (Khan et al. 1992).

Other hormones and substances are also found in seminal fluid such as, edothelin which facilitates transportation of sperm and also enhance sperm movements through the uterus by myometrial contraction stimulation(casey et al. 1992). The same is the case with bradykinin which helps transporation by its smooth muscle relaxing properties (Charlse Worth et al. 1999).

1.2 Which metals have been found in seminal fluid and why?

The interaction between metals and biomolecules are significant in biological systems. Metals determine many metabolic reactions and can also act as the aetiological agents in environmentally induced neurological disorders.

Traces of aluminium, zinc, magnesium, calcium and lead can be found in seminal fluid in bound ionic form. These metals are naturally found in minor traces and have an array of effects and uses and are collected in different avenues. It has been suggested that heavy metals may have adverse impacts on male reproductive health (Benoff et al., 2000) even at relatively low exposures (Telisman et al., 2007). The heavy metals may adversely affect the male reproductive system, either by inducing hypothalamic-pituitary axis disruption or by direct semen quality reduction during spermatogenesis (Wyrobek et al 1997)

Several metals are suspected endocrine disruptor compounds and/or reproductive toxicants such as mainly lead (Pb) and cadmium (Cd). Human populations could be exposed to heavy metals at trace concentrations usually through intake of contaminated water and food or contact with contaminated air or soil.

Blood and seminal Pb concentrations as well as semen quality among both occupationally exposed and unexposed men has been studied and concluded to have a significant inverse association [De Rosa et al 2003; Jurasović et al., 2004; Telisman et al., 2000, Eibensteiner et al., 2005]. Cadmium has been connected to impaired semen quality and altered hormonal levels in men [Pant et al 2003, Telisman.S et al, 2000, Akinloye et al., 2006; Zeng et al., 2002] . Although Cd has been considered as an endocrine disruptor, the mechanisms involved are not yet clear [Henson et al., 2004]. Mercury (Hg) has been found to induce abnormalities in sperm morphology and motility in animal vito studies [Mohamed et al., 1987; Rao et al., 1989]. [Choy et al., 2002] described Hg concentrations in seminal fluid and sperm abnormalities in subfertile males. But contrary to that, Meeker et al., 2008 discounted that claim after finding no relationship between semen quality and Hg levels in blood.

http://www.ehjournal.net/content/10/1/6

Zinc

The purpose of seminal plasma zinc on sperm functions has been a topic of interest to many scientists. Zinc organs from the prostate is well established and found in seminal plasma as zinc citrate or bound to glycoprotein derived from seminal vesicles (Marmar et al. 1975, Arver 1982, Arver and Eliasson 1982; Kavanagh 1983; Lafond et al. 1986) has been recognised since 1921 (Bertrand and Vladesco, 1921)

It has been found that zinc is essential to the decondensation of chromatin at the right time as well as stability. (kvist et al. 1987,1988). Zinc is thought to play a role as a preserver of an inherent mechanism for head-tail detachment of spermatozoa (Bjorndahl and Kvist, 1982). The total benefit or harm of zinc is obscure because it has been reported that high levels of zinc concentrations have been related to lowered sperm mortality, whilst others have reported that high zinc content in seminal plasma to be associated with a high degree of sperm cell motility (Stankovic and Mikac-Devic, 1976; Caldamone et al. 1979).

Zinc deficiency is associated with hypogonadism and insufficient development of secondary sex characteristics in humans (Prasad, 1991). Also high zinc concentrations have been reported to depress oxygen uptake in the sperm cell (Huacuja et al., 1973; Foresta et al., 1990), and albumin-induced acrosome reaction (Foresta et al., 1990). Zinc has also been found to be responsible for the antibacterial activity of seminal plasma (Fair et al., 1976) and reductions in levels are seen in prostatic infections (Marmar et al., 1975, Abyholm et al. 1981; Papadimas et al., 1983).

Sorensen et al., 1999, found higher levels of the total zinc content in semen from mammals, and they found the total zinc levels to be crucial to spermatogenesis. But zinc can also cause atrophy of the seminiferous tubules in the rat and resulting in the failure in spermatogenesis (Millar et al., 1958; Underwood, 1977; Endre et al., 1990). Consequently there have been conflicting reports on the effect of seminal zinc on sperm motility (Stankovic and Mikac-Devic, 1976; Danscher et al., 1978; Caldamone et al., 1979; Lewis-Jones et al., 1996). One such conflict arose when it was demonstrated that chelation of zinc ions has been found affecting the sperm motility (Saito et al., 1967; Danscher and Rebbe, 1974), and it has been suggested that bioavailable zinc bound to vesicular high molecular weight proteins rather than total seminal zinc should be a measure of the effect of zinc on sperm function (Bjorndahl et al., 1991; Carpino et al., 1998).

http://molehr.oxfordjournals.org/content/5/4/331.full.pdf+html

Like zinc magnesium also originates mainly from the prostate gland and the levels of this element in seminal plasma reflect prostatic function (Eliasson and Lindhomer, 1972). The magnesium levels usually closely correlate with those of zinc concentrations (Adamopoulos and Deliyiannis, 1983).Lead a metal best known for being environmentally harmful making it teratogenic and abortifacient. Lead administration in animals causes infertility. Lead is not naturally present in high amounts in the body but can be increased due to industrial exposure. The lead exposure has been observed to cause teratospermia and to display positive correlation to blood lead levels (Lancranjan et al.1975).

Seminal fluid is rich in calcium and helps regulate sperm function as the concentration of calcium in semen determines sperm motility, the ability of sperm to move. However studies show that an increased concentration of calcium ion was detrimental to human sperm motility.Calcium is important for sperm physiology including motility (Morton et al., 1974; Lindemann et al., 1987), metabolism (Peterson and Freund, 1976), acrosome reaction, and fertilization (Yanagimachi and Usui, 1974; Yanagimachi, 1981). The role of seminal calcium in sperm motility is, however, not fully understood. Thomas and Meizel (1988) found chelation of extracellular calcium ions with EGTA to inhibit acrosome reaction, but at the same time to have no effect on motility.Metals are ubiquitous at low level concentrations and are ingested by the general population either voluntarily through supplements or involuntarily through intake of contaminated food and water or contact with contaminated soil, dust, or air.

Some metals, such as cadmium, lead, arsenic, and mercury, are nonessential xenobiotics that can be measured in most of the general popu- lation [Centers for Disease Control and Prevention (CDC) 2005]. Because widespread human exposure and body burden have been demonstrated, there is growing concern for adverse health effects associated with low-level exposures encountered in the environment. Human and animal evidence suggests that these metals may have adverse impacts on male reproductive health at relatively low lev- els. For example, Cd has been linked to poor human semen quality and DNA damage (Telisman et al. 2000; Xu et al. 2003); Pb may adversely affect sperm shape, motility, and DNA integrity (Eibensteiner et al. 2005; Hernandez-Ochoa et al. 2005; Jurasovic et al. 2004; Telisman et al. 2007); and methyl- mercury is associated with sperm abnormalities in subfertile males (Choy et al. 2002). However, human data on nonoccupational

Exposure to these metals has been limited (e.g., Hg), lacking (e.g., As), or inconsistent across studies (e.g., Cd ). We designed the present study to explore relationships between these nonessential metals and semen quality among men with exposure levels that are likely to be representative of those found among the U.S. general population.

Several other metals, such as chromium, copper, manganese, molybdenum, selenium, and zinc, are essential for good health but may be harmful above certain levels [Agency for Toxic Substances and Disease Registry (ATSDR) 2003, 2004, 2005; Greger 1999; Institute of Medicine (IOM) 2001]. For exam- ple, Cr, Mn, and Cu, which act as cofactors for a variety of important enzymes, have been associated with reduced semen quality in rodents and in humans (Adejuwon et al. 1996; Huang et al. 2000; Kumar et al. 2005; Telisman et al. 2000; Wirth et al. 2007). Mo is also an important cofactor for a limited num- ber of human enzymes and has demonstrated reproductive toxicity in animal studies (IOM 2001). On the other hand, low doses of metals such as Cu, Se, and Zn may have protective effects on male reproductive outcomes (Benofft al. 1997; Evenson et al. 1993; Lyubimov et al. 2004; Olson et al. 2005) and may assist in counteracting the effects of Cd, Pb, or other metals (Telisman et al. 2000; Xu et al. 2003). Because the potential exists for a number of metals to positively or negatively affect male reproduction either individually or together, we also included these metals in our analysis. This wk represents the most comprehensive study to date on metal exposures at environ- mental levels and human semen quality.

http://www.scribd.com/doc/7905524/Cadmium-Lead-and-Other-Metals-in-Relation-to-Semen-Quality-Human-Evidence-for-Molybdenum-as-a-Male-Reproductive-Toxicant

Table 1.1 showing the effects of different metals on male reproductive system

The table below shows what Marthur and her colleagues found on how different metals affect the human male and male animals' reproductive systems.

Table taken from Journal of Biological Science by Marthur et al., 2010

The human race is becoming more and more industrialized and concurrently urbanized. This is one of many factors which has induced the effects of ionic bound metals in male reproductive systems and caused worldwide alert (Chowdhury, 2009; Turgut et al. 2003). Marthur et al., 2010 were looking at one of the most toxic and adverse effects with in the human males reproductive system.

An influx in raw materials consumption rates and scale has made the presence of metal compounds in the environment ever more ubiquitous. Anthropogenic activities have been established as one of the leading causes for ecotoxicological effects. Metals are versatile in composition and toxic ending points, so they cannot share an exact chemical basis in toxicology. Metals in ionic form have a tendency to be sensitive and highly reactive which means that they can react with biological elements, such as the human male reproductive system in a number of different ways. This in effect allows exogenous metals to exert toxic effects that are directly linked to steric re-arrangement which has been found to be responsible for biomolecule mal function. (Kasprzak, 2002 and Kasprzak et al., 2003).

After ingestion, metals can easily flow to the male reproductive system where the process of spermatogenesis is left vulnerable to alterations. Similarly, the metals can interact and react with genetic makeup of the human male hormones. Low sperm mortality and has been established to be a direct result of exposure to metals.

Looking back at this review it can be easily deduced that the toxicity and sensitivity of metals can be largely attributed to the hormonal alteration and spermatogenesis disruption and or malfunction.

(http://scialert.net/fulltext/?doi=jbs.2010.396.404&org=11)

1.3 A brief introduction to aluminium

Aluminium can be found bountifully in our environment. It is the third most abundant element in the Earth's crust, representing 8% by weight of the total components (Martin, 1997). The humans are inevitably and constantly exposed to aluminium. High contents of aluminium can be found in some rocks after the lithospheric cycle where it is introduced into the earth's crust. Weathering of these rocks is what causes aluminium-rich minerals to dissolve, which forms insoluble clay-like materials that eventually are re-introduced into the Earth's crust by sedimentation. Aluminium returns into the magma by further subduction, which in turn completes the cycle (Exley, 2003)

The resultant clay like materials play a significant role in the lithospheric cycle of aluminium so efficient (Exely, 2003) these along with the hydroxyaluminosilicates, galvanize the aluminium content so that it does not over concentrate the biotic cycle.

Usually aluminium enters the brain through the blood-brain barrier (BBB). It is suspected that the aluminium enters the brain by receptor-mediated endocytosis as a compound with transferrin (Roskams and Connor, 1990). it has been reported that aluminium can enter into the brain as a compound with transferrin which is bound to citrate through a specific transporter, Xc− (l-glutamate/l-cysteine) system exchanger is the most likely agent as explained by Nagaswa. (Nagasawa et al 2005). High aluminium intake has been related to the appearence a neurodegenerative disease (Perl&Moalem, 2006; Kawahara, 2005).

Aluminium has no biological benefit (Yokel 2002). It is a toxicant associated with some medical conditions such dialysis encephalopathy (Alfrey et al., 1976), osteomalacia (Parkinson et al., 1979), and it has been found to have links with many other diseases including Alzheimer's disease (Exley 1999; Gupta et al., 2005), Parkinson's disease (PD; Yasui et al., 1992), and amyotrophic lateral sclerosis (Kurland, 1988).

1.4 How are humans exposed to aluminium?

There are several avenues which humans can be exposed to aluminium due to its natural abundance in the environment. Traces can be found in food, water and air and even more amounts can be deliberately introduced by humans (Miller et al., 1984; Cech and Montera., 2000; Lettermann and Driscoll., 1988). Aluminium compounds can be found in pharmaceuticals like antacids, analgesics and antiperspirants. They are also used in water treatment processes as coagulants and can even be found as metal in everyday consumer products like foil paper and take away food boxes. Aluminium compounds are also found in nearly all plants. Edible plants that are naturally high in aluminium include potatoes, spinach and tea leaves (WHO, 1998). A recent study at Keele University also warned that unnecessarily high amounts of aluminium are being used in the manufacturing of infant powdered milk and that the aluminium content of formulas prepared from powdered milks was significantly higher than ready-made milks, resulting in infants ingesting up to 600 μg of aluminium per day Exley and Burrell, 2010. Pregnant women may be potentially exposed to aluminium through the diet (including drinking water), dust and soil ingestion and some medications (Roig et al., 2006). Studies have proven that aluminium is a major contributor to pathologies such as dialysis dementia, iron-adequate microcytic anaemia, osteomalacia ([Suwalsky et al., 2004] and [Domingo, 2006]) Over the past forty years the controversial question concerning the possible role for aluminium neurotoxicity in contributing to the pathogenesis of Alzheimer's disease has been debated but remains unresolved.

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TCN-4P6VDVC-2&_user=128592&_coverDate=10%2F08%2F2007&_rdoc=1&_fmt=high&_orig=gateway&_origin=gateway&_sort=d&_docanchor=&view=c&_acct=C000010620&_version=1&_urlVersion=0&_userid=128592&md5=ab46010ee2e9fa0fa7782f2dba6ebd0e&searchtype=a

1.5 What do we already know about aluminium and seminal fluid

So far I have found out that although aluminium is mostly a harmful metal with no direct biological benefit (Yokel, 2002), it is found in abundance in our environment. (Martin, 1997).Aluminium in high concentrations was linked to decreased sperm motility ability (Hovatta et al., 1998). It is also responsible for impaired sperm quality. Research was undertaken to discover the underlying discrepancies between sperm quality and geographic location by Hovatta and colleagues. Due to lack of clarification as to factors causing the decline, studies to examine semen quality and the concentrations of aluminium, cadmium and lead in spermatozoa and seminal plasma in a group of employees of a refinery and a polyolefin factory and the results were compared with data obtained from samples from sperm bank semen quality (Hovatta et al.,1998).

Research done in Finland discovered that high and unchanged sperm counts have been found (Suominen and Vierula, 1993; Vierula et al., 1996). In contrast to that, two necropsy series of middle-aged Finnish men showed an increase in the incidence of disorders of spermatogenesis between the years 1981 and 1991 was unveiled (Pajarinen et al., 1997). Meanwhile, decreased fertility in Britain ran parallel with that in Finland, based on differences in the time to conception (Joffe, 1996). Regional differences were also evident in the USA, with the highest average sperm concentration being found in New York (131.03106/ml) and (© European Society for Human Reproduction and Embryology) 115 the lowest in California (72.73106/ml) (Fisch et al., 1996). A small increase in sperm concentration between the years 1972 and 1993 was seen in Seattle, Washington (Paulsen et al., 1996).

It has been suggested that environmental factors played a role in the decline observed in Europe, especially environmental oestrogens (Sharpe and Skakkebaek, 1993). Oestrogens have also been suggested to have caused the increase seen in the incidence of cryptorchidism and testicular cancer (Sharpe and Skakkebaek, 1993; Skakkebaek and Keiding, 1994). Heavy metals are potentially pollutants that may be harmful to sperm production. Exposure due to occupation or geography to several metals is known to impair sperm quality (Schrag and Dixon, 1985). Substances such as lead and cadmium concentrations have been measured in human semen, seminal plasma, spermatozoa, blood and urine, and high concentrations have been found to be related to impaired sperm quality (Lancranjan et al., 1975; Plechaty et al., 1977; Braunstein et al., 1978; Pleban and Mei, 1983; Stanwell-Smith et al., 1983; Thomas and Borgan, 1983; Saaranen et al., 1987, 1989; Chia et al., 1992; Hu et al., 1992; Xu et al., 1993). In several experiments, many metals have also been shown to be harmful with regard to testicular function and sperm production (Alabi et al., 1985). Aluminium may well be one of the potential pollutants, because it reduces the weight of the testes and was seen to cause decreased epididymal sperm counts in the mouse (Llobet et al., 1979).

When aluminium is ingested in large amounts, it leads to accumulation in certain target organs such as the human and animal testicular tissues which results in damage occurring. The of long-term consumption of aluminium showed suppressive effects on sexual behaviour, decrease in fertility and aggressive behaviour (Bataineh et al., 1998). There is evidence implicating androgenic hormones involved in mechanisms of aluminium toxicity on male reproduction (Sharpe, 1990). To add to that, Guo et al. (2005a) carried out tests that proved that aluminium administration significantly increased nitric oxide (NO) production and decreased both testicular adenosine 3′,5′-cyclic monophosphate (cAMP) and testosterone levels. They demonstrated that excessive NO activated inducible NO synthase (NOS) which may be involved in reproductive toxicity of aluminium.

Information concerning the reproductive toxicity and testicular dysfunction of aluminium still needs more research. Also, the role of propolis against aluminium induced deteriorations in the reproductive ability of rats has not yet been discovered. The study taken on by (Yousef and Salama,2009), was aimed at determining the reproductive toxicity of aluminium chloride in adult male rats. It showed that aluminium enhanced lipid peroxidation in plasma, testes, brain, kidney, lung and liver of rabbits, and also in culture of rabbit sperm ([Yousef, 2004], [Yousef et al., 2005] and [Yousef et al., 2007]). Also, to evaluate the protective effect of propolis against the possible testicular dysfunction caused by aluminium chloride.

Table 1. Relative weights (g/100 g body weight) of sex organs of male rats treated with AlCl3, propolis and AlCl3 + propolis.

Parameter

Experimental groups

Control

AlCl3

Propolis

AlCl3+Propolis

Testes

0.72 ± 0.093

0.58 ± 0.061**

0.78 ± 0.0739***

0.66 ± 0.091*

Seminal vesicle

0.35 ± 0.061

0.20 ± 0.081**

0.39 ± 0.105***

0.31 ± 0.119*

Epididymis

0.27 ± 0.036

0.19 ± 0.037**

0.30 ± 0.036***

0.24 ± 0.041*

Prostate

0.16 ± 0.023

0.14 ± 0.021

0.16 ± 0.017

0.15 ± 0.02

Full-size table

Values are expressed as means ± SD; n = 10 for each treatment group. Significant difference from the control group at **P < 0.01.

Treatment of male rats with AlCl3 significantly (P < 0.01) decreased sperm concentration and motility rate. Meanwhile increased dead and abnormal sperm, as compared to control and propolis groups were seen in Table 2. Treatment with propolis alone showed no significant effects on sperm concentration and motility. while caused significant (P < 0.05) decrease in dead and abnormal sperm compared to control group. On the other hand, treatment with propolis in combination with AlCl3 caused significantly alleviated the decline in sperm concentration and motility, and significantly decreased the percentage of dead and abnormal sperm compared to AlCl3 group. This means that propolis minimized the toxicity of AlCl3.ignificant difference from the AlCl3-intoxicated group at #P < 0.05 and ##P < 0.01.

Table 2. Changes in sperm concentration (Sp. Conc., Ã-106/ml), motility (%), and dead (%) and abnormal (%) sperm of male rats treated with AlCl3, propolis and AlCl3 + propolis.

Parameter

Experimental groups

Control

AlCl3

Propolis

AlCl3 + Propolis

Sp. Conc.

212 ± 15.5

148 ± 8.1**

233 ± 12.1##

199 ± 7.5##

Motility

72.4 ± 1.89

50.9 ± 2.64**

79.7 ± 1.64##

70.5 ± 1.43##

Dead

25.2 ± 1.95

45.1 ± 2.21**

20.2 ± 1.78*##

28.8 ± 3.01##

Abnormal

14.6 ± 1.96

21.3 ± 2.312**

11.6 ± 1.27*##

16.7 ± 1.337##

Full-size table

Values are expressed as means ± SD; n = 10 for each treatment group.Significant difference from the control group at *P < 0.05 and **P < 0.01.Significant difference from the AlCl3-intoxicated group at #P < 0.05 and ##P < 0.01.

This study observed the effect of aluminium chloride on sperm motility. (Table 2). Additionally, Dawson et al., 1998 E.B. Dawson, S. Ritter, W.A. Harris, D.R. Evans and L.C. Powell, Comparison of sperm viability with seminal plasma metal levels, Biol. Trace Elem. Res. 64 (1998), pp. 215-223.Dawson et al. (1998) found that high concentrations of aluminium in human spermatozoa and seminal plasma are correlated with decreased sperm motility and viability. Motility is crucial in enabling the sperm to swim through the female reproductive tract and reach the ovum to achieve fertilization (Aitken, 1995). The observation can be concluded by saying that the decrease in sperm motility was caused in part to the concomitant reduction in testosterone production ([Guo et al., 2005a] and [Yousef et al., 2005]) following aluminium treatment.

Table 3. Plasma testosterone concentration (ng/ml) and activity of testicular 17- ketosteroid reductase enzyme (U/min/mg protein), and testes protein content (mg/g tissue) of male rats treated with AlCl3, propolis and AlCl3 + propolis.

Parameters

Experimental groups

Control

AlCl3

Propolis

AlCl3 + Propolis

Testosterone

1.31 ± 0.244

1.00 ± 0.115*

1.51 ± 0.113*#

1.15 ± 0.064#

17-Ketosteroid Reductase enzyme

14.6 ± 2.02

10.2 ± 1.13**

19.1 ± 1.49**##

12.8 ± 2.03*#

Protein content

76 ± 4.4

60 ± 4.7**

105 ± 5.3**##

75 ± 5.2##

Full-size table

Values are expressed as means ± SD; n = 10 for each treatment group.Significant difference from the control group at *P < 0.05 and **P < 0.01.Significant difference from the AlCl3-intoxicated group at #P < 0.05 and ##P < 0.01.

Data in Table 3 showed significant decrease in plasma testosterone concentration (P  0.05) and testicular protein (P  0.01) in rats treated with AlCl3 compared to control. While, propolis significantly increased testosterone and protein content and alleviated the negative effects for AlCl3 in group 4 on these parameters.

Aluminium chloride exposure displayed gonadotoxic effects in male rats and maternal death was associated with fetal death in pregnant rats. The exposure to aluminium increases the incidence of foetal abnormalities in rats and mice (Belles et al., 1999). The study of Guo et al. (2005a) demonstrated that exposure to aluminium lowered plasma and testicular testosterone levels in mice. It was suggested that the severe reduction in male libido and fertility following the aluminium administration might be a result from excessive aluminium accumulation in the testes and low testosterone concentrations. High levels of aluminium in aluminium-treated mice were apparent at week 3 before the effects on male libido and fertility manifested. The discrepancy was reasoned such that aluminium accumulation failed to immediately affect the enzymes for androgen biosynthesis or produce a possible disturbance in hypothalamic-pituitary-gonadal axis. However, the present study showed that AlCl3 caused significant decline in the activity of 17-ketosteroid reductase after 70 days treatment (Table 3).

Table 4. Changes in the activities of catalase (CAT; mol/h/g tissue) and glutathione S-transferase (GST; μmol/min/g tissue), and the levels of thiobarbituric acid-reactive substances (TBARS; nmol/g tissue) and reduced glutathione (GSH; mM/g tissue) in testes of rats treated with AlCl3, propolis and AlCl3 + propolis.

Parameter

Experimental groups

Control

AlCl3

Propolis

AlCl3+Propolis

CAT

6.96 ± 1.140

3.01 ± 0.578 **

9.95 ± 1.050 **##

5.89 ± 0.793 ##

GST

1.08 ± 0.100

0.59 ± 0.154**

1.43 ± 0.299 **##

0.96 ± 0.125 ##

TBARS

71.8 ± 5.58

195.9 ± 10.62 **

60.4 ± 6.18 *##

97.4 ± 9.58 *##

GSH

6.02 ± 0.694

4.15 ± 0.690 *

8.25 ± 0.902 *##

5.74 ± 1.863 #

Full-size table

Values are expressed as means ± SD; n = 10 for each treatment group.Significant difference from the control group at *P < 0.05 and **P < 0.01.Significant difference from the AlCl3-intoxicated group at #P < 0.05 and ##P < 0.01.

The control testes are surrounded by a dense fibrous tissue capsule known as the tunica albuginea The histological study showed that.The testies are divided into lobules by thin fibrous septa; the interstitial tissue surrounds the lobules which contain several seminiferous tubules within them. The tubules are lined with germ cells in various stages of spermatogonia, some primary and secondary spermatocytes, spermatids and mature spermatozoa that occupy the centre of the tubule. Between the spermatogonia and the remainder of the basal lamina are the sertoli cells. The interstitial tissue is supported by Leydig cells in principal. They occur singly or in clumps and are embedded in the rich plexus of blood and lymph capillaries. Observations of testes treated with AlCl3 revealed several alterations. The accumulation of exfoliated germ cells within some seminiferous tubules affected their architecture and left them disorganized. Some tubules exhibited maturation arrest. And moreover, some germ cells had small and darkly stained nuclei. Marked dilation and congestion of blood vessels were noticed in the interstitial spaces. Hyperplasia of Leydig was detected in the interstitial tissue. The Leydig cells became crowded and formed dense clumps that surrounded most of the seminiferous tubules (Fig. 2). Some sections of testes of the rats treated with propolis alone showed that they were less or more similar to the control sections (Fig. 3). Testis of rats treated with aluminum plus propolis revealed that it regained almost all of its original structure and remarkable restoration of the normal picture of seminiferous tubules was attained. The germ cells appeared regular in shape with disappearance of most cytoplasmic vacuolation. Most of the nuclei became vesicular (Fig. 4). Testes accumulate high aluminum over age in rats (Gomez et al., 1997). Light microscopy of silver-stained paraffin sections of the testes demonstrated numerous intracytoplasmic black-stained fine granular inclusions in Leydig cells (Reusche et al., 1994). The histological changes in testes of rats treated with AlCl3 (Fig. 2) is concurrent with the obtained data by Khattab (2007) who studied the effect of AlCl3 on the testes of rats after an intraperitoneal injection was administered. The testes showed histological perturbation including severe damage within the seminiferous tubules and vascular degeneration on the spermatogenic and sertoli cells cytoplasm. The germinal epithelium of the seminiferous tubules was thinner in places and spermatids became very scarce in presence. Sperm numbers was low and there were no sperm in the lumen. Also, up on electron microscopic studies, in the aluminium-treated group, there were some anomalies in the nuclear membrane, damages to some mitochondria, ribosomes population decrease, and an increase in the number of lysosomes in the sertoli cell cytoplasm. In the primary spermatocyte cytoplasm, there was an increase in the rough endoplasmic reticulum. Guo et al. (2005b) found that after 2 weeks of aluminium treatment, deleterious effects and histopathological changes of testicular tissues were observed. However, noticeable spermatogenetic loss was viewed as necroses in the spermatids and spermatozoa in aluminium-treated group at week 5. The impairment caused by aluminium was accompanied primarily by the prolonged accumulation of aluminium in the mice testest.

Fig. 1. Photomicrograph of control testis section showing interstitial cells (I) and germ cells (G). H&E stain (400Ã-).

Fig. 2. Photomicrograph of testis section that treated with aluminium showing germ cells (G), exfoliated germ cells (E), hyperplasia of Leydig cells (I) and vacuolation (V). H&E stain (400Ã-).

Fig. 3. Photomicrograph of testis that treated with propolis showing germ cells (G). H&E stain (400Ã-).

Fig. 4. Photomicrograph of testis section that treated with Aluminium and propolis showing germ cells (G). H&E stain (400Ã-).

1.6 Aims and objectives of my project

In this project my main aim was to determine the presence of aluminium in seminal fluid and spermatozoa. I had to found out if aluminium was present in the seminal fluid or the spermatozoa.

Discussion

THE EFFECT OF ORAL HIGH ALUMINIUM INTAKE ON RAT SPERMATOGENESIS

I.M.D. Rashidi. Head of department & member of expert committee Dept of pathology Medical school Ahwaz medical university, Ahwaz IRAN

Aluminium is one of the most abundant elements in the earth crust and enters to the body through drinking water,nutrients and drugs like antiacids. Aluminium poising causes wide range of disorders, including: a decrease in the release of neurotransmiters and inhibition of voltage dependent calcium channels. The role of calcium on GnRH release and its action is detected so, in this studying, the effect of high aluminium intake on rats spermatogenesis is investigated.

The experiment performed in four groups, a control group

and three experimental groups consumed 0.625, 1.25 and 2.5 mg aluminium per gram diet for 60 days. Epididymis and vas deferens were dissected cut and diluted with normal salin. In all groups weight of vas deferens, epididymis, testis and whole animal, sperm count per gram deferens and epididymis tissues were determined then, the testicular tissues fixed in formalin for study of histopathology.

The results have shown that in experimental groups which consumed 1.25 and 2.5 mg aluminium per gram diet, the vas deferens, epididymis, testis and animal weight were significantly decreased. In this animals the number of sperm per gram tissues from vas deferens, epididymis were reduced. The maturation arrest is seen in seminoferous duct and it haven't spermatogenesis. Therefore, this studying indicated that high aluminium intake in rat have an inhibiting effect on spermatogenesis and this effect is dose dependent.

http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6TCR-4CB7K82-GF-1&_cdi=5177&_user=128592&_pii=S0378427403904048&_origin=gateway&_coverDate=09%2F28%2F2003&_sk=998559999.8998&view=c&wchp=dGLzVtb-zSkzV&md5=1f1a3377fb5ad50ff2bd8ffd8947d810&ie=/sdarticle.pdf

Read and summarise but reference

http://humrep.oxfordjournals.org/content/13/1/115.full.pdf

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