Mercury induced ­histopathological changes in the ovary of the freshwater fish, Rasbora dandia

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Mercury induced ­histopathological changes in the ovary of the freshwater fish, Rasbora dandia

Introduction

Aquatic ecosystems are under continuous pressure from pollutants of anthropogenic origin. Being one of the important vertebrate species of water bodies and due to its top position in the aquatic food web, the fish species are the biotic form which are most affected by the pollutants. Xenobiotic effects of these chemicals often adversely affect fish reproduction and directly cause massive damage to the fish populations.

Among the industrial pollutants, heavy metals pose great concern as they are persistent, highly toxic and many of them bioaccumulates and biomagnifies. Among the heavy metal pollutants, mercury is more dangerous being a neurotoxin and it may be converted to a more potent form methyl mercury. Even at low concentration, mercury may affect fish population through impairment of physiological processes like reproduction (Crump and Trudeau, 2009). Kidd and Batchelar (2012) pointed out that it is not understood how chronic mercury exposure affects the reproductive success of wild fish. Although toxicity of heavy metal mercury is well established, the ecotoxicology of mercury is an area of substantive scientific discovery. Further, comparative toxicity data linked to reproductive endpoints are limited for most taxonomic classes of vertebrate organisms. Such information aid in identifying mercury sensitive species and at-risk populations (Wiener, 2013). The present study is our attempt to evaluate the histopathological changes in the ovary of Rasbora dandia induced by mercury.

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Materials and methods

Rasbora dandia were collected from freshwater bodies of Thrissur, Kerala. These fishes were transported to the laboratory carefully and acclimatized to the laboratory conditions. Fishes with almost 5.5 to7.5 cm length and 2.5-5.5 gm weight are selected and 10 fishes were kept in each aquarium. Mercuric chloride was used as source of the mercury. To calculate lethal concentration, fishes were exposed to 80, 100, 120, 140 and 160 ppb of mercury. Number of mortality in each aquarium is recorded on every 12 hours for a period of 96 hours. From this reading, LC50 value was found out using probit analysis. 96 hours LC50 concentration of mercury was found to be 133.3 ppb of Hg.

Experimental fishes were exposed to sublethal concentration of 10 ppm of mercury for 30 days. Test solutions are renewed every 24 hours and fed with standard fish feed. Fishes were anaesthetised and scarified on every 10 days time interval during the experiment. Ovaries were dissected out and placed in Bouins’s fluid for fixation. Ovaries were dehydrated in ethanol and cleared in methyl benzoate. Specimens were then infiltrated with paraffin wax and embedded in paraffin blocks. 6 m sections were taken using rotary microtome and stained using haematoxylin and eosin. Histopathological changes were observed under light microscope. Changes in the frequency of different stages of oocytes were evaluated after every 10 days exposure period. 300 cells were considered from various histological sections of the ovary and classified on the basis of developmental stage as immature oocytes, maturing oocytes and mature oocytes. Gonadosomatic index (GSI) was calculated using the method followed by Kirubagaran and Joy (1988). Student’s t-test was used for statistical analysis of GSI.

Results and discussion

Gonadosomatic index was found to progressively decline as the exposure period of mercury increases (Table 1). Histopathological changes appeared in the ovary of the fish from 10 days of mercury exposure. Mass atresia of oocytes occurred resulting in huge loss of oocytes in the ovaries (Fig. 6). On the 30th day, it is observed that most of the vitellogenic oocytes are destroyed and immature oocytes become predominant in the ovary (Fig. 7). Gradual decline in the percentage of maturing and mature oocytes by mercury exposure are shown in the (Fig. 1, 2, and 3). Ripe ovaries transformed in to shrunken immature ovaries with histopathological alterations (Fig. 4, 5, 6, and 7).

Irregularly shaped oocytes and blebbing of oocyte membranes were appeared in the ovaries of mercury treated fishes (Fig. 10). Mature oocytes undergo atresia by resorption of yolk and convolution of oocyte membranes (Fig. 9). Immature ovaries undergo atresia by the formation of large vacuoles in the cytoplasm. These vacuoles later join together and invade nucleus (Fig. 8). Areas devoid of oocytes appeared in the ovary where appearance of fibrotic tissue occurred (Fig. 7).

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Table 1. Effect of mercury exposure on GSI of female Rasbora dandia (Mean± SD)

Exposure period

Control fishes

Fishes exposed to10 ppb mercury

10 days

19.017± 0.98

12.47± 1.12*

20 days

19.73± 1.35

7.29± 0.37*

30 days

19.23± 0.74

4.19± 0.23**

* Significant at p0.01, **Significant at p0.001

In teleosts, immature or previtellogenic oocytes transform into mature oocytes through the accumulation of yolk vesicles (Tyler and Sumpter, 1996). Cytotoxic pollutants can interfere with normal physiology of ovaries resulting in various degenerative changes in the ovary. Adams et al., (1999) observed the increase in the frequency of atretic oocytes with sediment mercury concentration in largemouth bass. They observed increase in the frequency of atretic oocytes in sexually mature largemouth bass with increase in sediment mercury concentrations.

Dey and Bhattacharya (1989) reported the preponderance of early stage oocytes and destruction of advanced stages of oocytes in the ovary of Channa punctatus after chronic exposure to low concentrations of mercury. Masud et al., (2009) reported over-all reduction on oocyte development in the ovary of Cyprinus carpio after short term exposure to safe concentration of mercuric chloride. Kirubagaran and Joy (1988) observed decreased GSI, impaired vitellogenesis and degenerative changes in the oocytes in the ovaries of Clarias batrachus exposed to mercuric chloride, methyl mercuric chloride and emisan 6. In the present study, as the duration of exposure period increases the percentage of mature oocytes declines in the ovary of Rasbora dandia (Fig. 1, 2 and 3). It indicates that oocytes in the advanced stages are more vulnerable to mercury. Along with the histopathological changes, gradual decline in GSI is observed under the influence of mercury (Table 1). The results show that chronic mercury exposure to fishes may cause ripe ovaries transform into shrunken immature ovaries with histopathological alterations (Fig. 4, 5, 6, and 7).

By 30 days of mercury exposure, huge loss of oocytes occurs by mass atresia in the ovary of the experimental fish, Rasbora dandia. Fibrotic tissue appeared in place of lost oocytes (Fig. 7). Kirubagaran and Joy (1988) reported extensive infiltration of fibroblast like cells in the ovary of Clarias batrachus exposed to mercuric chloride. Large scale depletion of oocytes as well as fibrosis can cause unrecoverable damage to the ovary induced by mercury. Sensitivity of advanced stages of oocytes to mercury exposure hinders reproductive success of fishes. Degenerative lesions in oocytes affect fish progeny both in number and viability. The present study indicates that in cases of acute exposures of mercury, irreversible changes in the gonads may occur resulting in sterile populations.

Acknowledgements

The first author is indebted to Council of Scientific & Industrial Research (CSIR), India for providing fellowship. We are grateful to Christ College, Irinjalakuda for providing laboratory facilities.

References

1. Adams, S. M., Bevelhimer, M.S., Greeley, M.S., Levine, D.A, and Teh, S.J. 1999. Ecological risk assessment in a large river-reservoir: 6. Bioindicators of fish population health. Environ. Toxicol. Chem., 18:628–640.

2. Dey, S. and Bhattacharya, S. 1989. Ovarian damage to Channa punctatus after chronic exposure to low concentrations of elsan, mercury, and ammonia. Ecotoxicol. Environ. Saf., 17:247–257.

3. Wiener, J. G. 2013. Mercury exposed: Advances in environmental analysis and ecotoxicology of a highly toxic metal. Environ. Toxicol. Chem.,32:10, 2175-2178.

4. Crump, K.L. and Trudeau, V.L. 2009. Mercury-induced reproductive impairment in fish. Environ. Toxicol. Chem., Vol. 28, No. 5, pp. 895–907.

  1. Kidd, K. and Batchelar, K. 2012. Mercury. In “Homeostasis and Toxicology of Non-Essential Metals” (C. M. Wood, A. P. Farrel, and C. J. Brauner, eds.), Fish physiol. 31B, 125-184.

6. Kirubagaran, R. and Joy, K.P. 1988. Toxic effects of mercuric chloride, methylmercuric chloride, and Emisan-6 (an organic mercurial fungicide) on ovarian recrudescence in the catfish Clarias batrachus (L.). Bull. Environ. Contam. Toxico., 41:902–909.

7. Masud, S. Singh, I.J. and Ram, R.N. 2009. Histopathological responses in ovary and liver ofCyprinus carpioafter short term exposure to safe concentration of mercuric chloride and recovery pattern. J. Environ. Biol., 30:399–40.

8. Tyler, C.R. and Sumpter, J.P. 1996. Oocyte growth and development in teleosts. Rev. Fish Biol. Fish., 6:287–318.

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