Investigation of Serum Enzyme Activity In Renal Tumors

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27th Sep 2017 Health Reference this

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Investigation of Serum Enzyme Activity of Nitric Oxide (NO), Arylesterase (ARE) and Paraoxanase (PON) In Renal Tumors

 

Abstract

Objectives: Reactive oxygen species (ROS) and antioxidant capacity have been implicated in the pathogenesis of various diseases, including cancers. Oxidative stress can cause tumor angiogenesis and may be carcinogenic. However, the relationship between antioxidant capacity and various cancers has been researched in several clinical trials. In our study, we aimed to identify serum Nitric Oxide (NO), Arylesterase (ARE) and paraoxonase (PON) activities in patients with renal tumors .

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Materials and Methods: A total of 32 male patients with renal cell cancer and with a mean age of 55.32 +2.9 were included in the study. The control group comprising 29 male patients (mean age 56.01 + 3.0) was randomly selected among the volunteers. Serum samples for measurement of Nitric Oxide (NO), Arylesterase (ARE) and Paraoxonase (PON) levels were kept at 20°C until they were used.

Results: Serum nitric oxide (NO) was determined to increase activity of cancer group. Serum Arylesterase (ARE) were significantly lower in the patient group than the control group. Serum paraoxonase (PON) activity was increased in the control group (all, p < 0.05). Conclusion: Our results indicate that Nitric oxide (NO), arylesterase (ARE) and paraoxonase (PON) activities play an important role in the pathogenesis of renal cell cancer.

Keywords: ARE, NO, PON, Renal tumor, Tumor marker.

Introduction

In the United States, approximately 30,800 new cases of renal cancer and 12,000 deaths from renal cancer are reported annually,making renal cancer the sixth largest cause of cancer deaths. Renal cell carcinoma accounts for 90–95% of all kidney malignancies (1). The incidence of renal cell carcinoma has been increasing in the United States and worldwide by approximately 2–4% per year, for the last 20 years (2,3). Advances in diagnostic imaging and early detection do not fully explain this trend. Rates of renal cancers are higher among males and have been increasing more rapidly among African Americans than Whites (2). Established risk factors for renal cancer include smoking, use of phenacetin containing drugs, hypertension, obesity, and end-stage renal disease (ESRD)(4). Of the patients who present with local disease and are considered for surgery with curative intent, approximately one third

will go on to develop metastatic disease. Metastatic kidney cancer is resistant to all ‘‘standard’’ forms of radiation therapy, chemotherapy, and hormonal therapies used in the treatment of other kinds of carcinomas.

Reactive oxygen species (ROS) have been implicated in the pathogenesis of various diseases, including cancers(5). In previous studies, it has been demonstrated that ROS are directly suggested in oxidative damage of cellular macromolecules such as lipids, proteins, and nucleic acids in tissues(6). Moreover, oxidative stress can lead to tumor angiogenesis. It has also been reported that ROS can also augment tumor cell migration, increasing the risk of invasion and metastasis(7).

However, the relationship between antioxidant capacity and various cancers has been investigated in several clinical trials. Ray et al. reported increased lipid peroxidation (LPO) and production of reactive oxygen metabolites (ROMs) and decreased activities of superoxide

dismutase (SOD) in breast cancer patients. Increased glutathione peroxidase (GSHPx) activity

also was reported by the same researchers(8). Vitamin E is a supporter of antioxidant system, and a supplementation trial conducted in China showed a significant reduction in stomach cancer mortality(9). Oberley and Buettner reported that the vast majority of the cancer cells have very low SOD activity, as compared with their normal cell counterparts(10). Gecit et al. reported that increased prolidase seems to be associated with increased nitric oxide (NO) levels and oxidative stress along with decreased antioxidant levels in bladder cancer (11).

In this study, we aimed to identify serum Nitric Oxide (NO), Arylesterase (ARE) and paraoxonase (PON) activities in patients with renal tumors .

Materials and methods

A total of 32 male patients with renal cell cancer with a mean age of 55.32 +2.9 were included in the study. All of the patients have not smoked during their life, they were not addicted to alcohol, have not used the supportive antioxidant, and did not abuse any drug and

have any metabolic disorders. There were no other major diseases or cancers in any of the patients except for the kidney tumor. All of the patients have been newly diagnosed, and their blood samples were received in the preoperative period. In all, 29 male patients who made up the control group (mean age 56.01 + 3.0) were randomly selected among the volunteers who did not have any known major disease and who did not use cigarettes, alcohol, drugs, and additional antioxidants. Patient and control groups had a similar socioeconomic status.

According to the results of radiological and postoperative histopathological evaluation, 24 (75%) of our patients were in stage 1, 6 (18.75%) of them were in stage 2, and 2 (6.25%) of them were in stage 4 of metastatic renal tumor.

The study protocol was carried out in accordance with the Helsinki Declaration as revised in 1989. All participants were informed about the study protocol and the written consent was taken from each one.

Blood collection;

Following 12 h of fasting period, blood samples were taken in the morning, collected into empty tubes, and immediately kept on ice at 4 °C. The serum was then isolated from the cells by centrifugation at 3000 rpm for 10 min. Serum samples for measurement of Nitric Oxide (NO), Arylesterase (ARE) and paraoxonase (PON) levels were kept at 20°C until they were used.

Methods of Analysis

Nitric Oxide (NO)

NO levels in serum was determined using the Griess reaction. Griess solution X: 0.1 g NED (N-1-naphthyl)-ethylenediamine dihydrochloride) was weighed and dissolved in 100 ml water. Again, Y Griess solution: 1 g sulphanilamide in 100 ml of orthophosphoric acid (5%) was dissolved in a solution. 100 mico liter sample was taken and each tube was placed in a 0.1 ml Griess solution X and 0.1 ml Griess solution Y equal to tubes placed in and stirred, then 15 minutes at room temperature was allowed to stand and each sample at 540 nm absorbance values ​​were read.

Arylesterase (ARE)

Arylesterase activity in 2004 and 2005, developed by Erel was determined with a kit. 10 μml onto 990 ml diluent solution was added 10/100 ratio dilutions were performed this diluted from the 3 μml enrolled over 260 μml pure water (Reagent 1) was added, then 10 μml Reagent 2 was added, then vortexed and at 548 nm enzyme activity was measured. Measurements are taken more spectrokuvet A1 80 μml Reagent 3 was added and again after waiting 4 minutes at 548 nm was measured and the measurements of activity is defined as A2. For activity measurement (enzyme unit) = (ΔA2-ΔA1) x1316.

Paraoxanase (PON)

Paraoxonase activity in 2004 and 2005, developed by Erel was determined with a kit. The two tubes are each 500 μml reagent 1 (buffer solution) was added and on 25 μml sample (serum) was added and stirred then 25 μml reagent 2 (substrate solution) was added 30 sec and 150 sec after the absorbance measurement at 412 nm was read. Activity measurement (U / L) = [(Δ150sn-Δ30sn) / 2] x1202.84

Statistical analysis

Descriptive statistics for the studied traits were expressed (reported) as mean, standard deviation, minimum, andÄ°statistiksel yorum maximum values. Student’s t test was used for comparison of groups. In the study, 5% level was taken into account to the statistically significant differences between groups, and SPSS Statistical package program (ver. 13) was used for the all statistical computations.

Results

The demographic and clinical data of bladder cancer and control groups are shown in Table 1. There were no statistically significant differences between renal cancer patients and controls with respect to age and body mass index (BMI) (all ps > 0.05; Table 1).

Serum NO level was significantly higher in renal cancer than in controls (all ps < 0.05); while ARE and PON levels were significantly lower (p < 0.05; Table 2). No correlation was observed between tumor staging and serum NO, ARE and PON levels (ps > 0.05).

Discussions

Biological and biochemical systems (CAT), peroxidase (POD), glutathione reductase (GSSG-Rx) and superoxide dismutase (SOD) are enzymes having antioxidant activity. Antioxidant defense system, cell free radical or other reactive molecules protects against oxidative damage. Therefore, this defense system, CAT, POD, PON, ARE, GSSG-Rx and antioxidant enzymes such as SOD is of great importance. The harmful effects of free radicals in cells are controlled by antioxidant defense systems.

Although some possible mechanisms through which oxidative stress exerts a regulatory role in tumor growth and progression including genomic instability, oncogene activation and angiogenesis are known, several important questions remain unanswered (12,13,14). It is not clearly known whether oxidative stres and tumor result from an increased oxidant production or from a failure of antioxidant systems (15). Although important changes in cellular redox homeostasis during tumor growth have been documented in experimental models, such variations have not been shown in humans. Most of the difficulties encountered in these studies are related to the complexity of the biochemical pathways that regulate the cellular redox balance (16,17). A wide variety of oxidizing molecules such as ROS and/or depleting agents can change the glutathione redox state, which is normally maintained by the activity of GSH depleting (GSH-Px) and replenishing enzymes (glutathione reductase). The importance of GSH and related enzymes and their variation in tumors has been poorly studied (16,13).

The enzymes eliminate oxygen free radicals of the cell plays an important role in the protection from oxidative damage. Antioxidant status and lipid peroxide and oxidized proteins well known marker of oxidative stress as measured by the relationship between the level and posture better reflects the health index. Cholesterol free radicals, arachidonic and deoksihegzanet binds to and initiates lipid peroxidation. One of the best indicators of this process has begun ROS can cause renal damage and cardiovascular disorders. In a study conducted in rats of cigarette smoke effects on antioxidant enzymes and lipid peroxidation has been studied, a significant increase in lipid peroxidation was observed that while no significant difference in antioxidant enzymes.

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Abnormal cell proliferation in the serum cancerous patient is the cause of lipid peroxidation (LP) increase. The increase in LP in cancer may also be owing to the poor antioxidant system as observed in the previous studies (18). It has been claimed that MDA acts as a tumor promoter and cocarcinogenic agent on account of its high cytotoxicity and inhibitory action on protective enzymes (19,20). The data reported in the literature on MDA levels in different human cancer types are controversial. On the other hand, MDA, the major aldehyde end product of LP of membrane polyunsaturated fatty acids by free radicals, is an indicator of oxidative stress (21). In the present study, we found a significantly increased serum MDA levels in patients with renal cancer than in control subjects.

The data reported in the literature on oxidant, antioxidant molecule, and enzymes in different human cancer types are controversial. For instance, in a study the activities of SOD and GSH-Px enzymes were found lower in malignant liver tissues during rat hepatocarcinogenesis (22). In another one, Corrocher et al. established that in human hepatoma the enzymatic antioxidant system was severely impaired owing to lowered GSH-Px activities (23). Nakada et al. measured SOD activities in renal cell carcinoma and nontumorous renal tissues (24). They found no meaningful differences between the activities of the cancerous and noncancerous parts and suggested that it was unlikely for SOD to play a part in the development of renal cell carcinoma since SOD activities in tumor tissue were similar to those in nontumorous renal tissues (24). Ray et al. observed a significant increase in SOD and GSH-Px activities in patients with gastric cancer compare to the control group (8). Ozturk et al. observed a significant increase in xanthine oxidase (XO) activity in patients with cancerous human colorectal tissues compared to control group (25). The increased GSH-Px activities and GSH levels are reported in patients with leukemia (26,27).

NO levels in prostate cancer patients is increased compared to healthy humants . NO studies may be related to tumor growth by two separate mechanisms. First, the stimulation of angiogenesis, and the other pole of DNA by the activation of free radicals is increased mutagenesis. In addition, the release of NO from tumor cells, through non antiproliferative effects may follow from a role in tumor-induced immunosuppression . The present our study supports in literature studies.

The reduction of antioxidant enzyme activity increases as a result of oxidative DNA damage, has been found to be proportional . In addition, in the literature study in coronary artery disease oxidative DNA level has been found increased . In our study group, serum ARE was significantly lower than the control group (p <0.001).

Conclusions:

According to the results of our study of patients with renal cell carcinoma was found a decrease in the antioxidant defense system. Oxidant / antioxidant balance of damage in the development kidney cancer might be considered a risk factor. This is relevant for the formation of a konsessus randomized prospective studies are needed.

Parameters

Patients (n= 32)

Controls (n=29)

Age, year

55.32 ± 2.9

56.01 ± 3.0

Body mass index, kg/m2

21.56 ± 1.86

21.33 ± 1.29

Table 1. Demographic characteristics of the two groups in this study.

 

Patients (n=32)

(XSx)

Control

(n=29)

(XSx)

p

NO (µmol/L)

8.397± 2.0981

1.192± 0.1474

<0.001

ARE (U/mL)

17.518±3.5288

42.170± 6.8991

<0.001

PON (U/mL)

57.570±7.2911

94.423±4.7110

<0.001

Table 2. Descriptive statistics and comparison results according to the groups for specifications.

References:

Investigation of Serum Enzyme Activity of Nitric Oxide (NO), Arylesterase (ARE) and Paraoxanase (PON) In Renal Tumors

 

Abstract

Objectives: Reactive oxygen species (ROS) and antioxidant capacity have been implicated in the pathogenesis of various diseases, including cancers. Oxidative stress can cause tumor angiogenesis and may be carcinogenic. However, the relationship between antioxidant capacity and various cancers has been researched in several clinical trials. In our study, we aimed to identify serum Nitric Oxide (NO), Arylesterase (ARE) and paraoxonase (PON) activities in patients with renal tumors .

Materials and Methods: A total of 32 male patients with renal cell cancer and with a mean age of 55.32 +2.9 were included in the study. The control group comprising 29 male patients (mean age 56.01 + 3.0) was randomly selected among the volunteers. Serum samples for measurement of Nitric Oxide (NO), Arylesterase (ARE) and Paraoxonase (PON) levels were kept at 20°C until they were used.

Results: Serum nitric oxide (NO) was determined to increase activity of cancer group. Serum Arylesterase (ARE) were significantly lower in the patient group than the control group. Serum paraoxonase (PON) activity was increased in the control group (all, p < 0.05). Conclusion: Our results indicate that Nitric oxide (NO), arylesterase (ARE) and paraoxonase (PON) activities play an important role in the pathogenesis of renal cell cancer.

Keywords: ARE, NO, PON, Renal tumor, Tumor marker.

Introduction

In the United States, approximately 30,800 new cases of renal cancer and 12,000 deaths from renal cancer are reported annually,making renal cancer the sixth largest cause of cancer deaths. Renal cell carcinoma accounts for 90–95% of all kidney malignancies (1). The incidence of renal cell carcinoma has been increasing in the United States and worldwide by approximately 2–4% per year, for the last 20 years (2,3). Advances in diagnostic imaging and early detection do not fully explain this trend. Rates of renal cancers are higher among males and have been increasing more rapidly among African Americans than Whites (2). Established risk factors for renal cancer include smoking, use of phenacetin containing drugs, hypertension, obesity, and end-stage renal disease (ESRD)(4). Of the patients who present with local disease and are considered for surgery with curative intent, approximately one third

will go on to develop metastatic disease. Metastatic kidney cancer is resistant to all ‘‘standard’’ forms of radiation therapy, chemotherapy, and hormonal therapies used in the treatment of other kinds of carcinomas.

Reactive oxygen species (ROS) have been implicated in the pathogenesis of various diseases, including cancers(5). In previous studies, it has been demonstrated that ROS are directly suggested in oxidative damage of cellular macromolecules such as lipids, proteins, and nucleic acids in tissues(6). Moreover, oxidative stress can lead to tumor angiogenesis. It has also been reported that ROS can also augment tumor cell migration, increasing the risk of invasion and metastasis(7).

However, the relationship between antioxidant capacity and various cancers has been investigated in several clinical trials. Ray et al. reported increased lipid peroxidation (LPO) and production of reactive oxygen metabolites (ROMs) and decreased activities of superoxide

dismutase (SOD) in breast cancer patients. Increased glutathione peroxidase (GSHPx) activity

also was reported by the same researchers(8). Vitamin E is a supporter of antioxidant system, and a supplementation trial conducted in China showed a significant reduction in stomach cancer mortality(9). Oberley and Buettner reported that the vast majority of the cancer cells have very low SOD activity, as compared with their normal cell counterparts(10). Gecit et al. reported that increased prolidase seems to be associated with increased nitric oxide (NO) levels and oxidative stress along with decreased antioxidant levels in bladder cancer (11).

In this study, we aimed to identify serum Nitric Oxide (NO), Arylesterase (ARE) and paraoxonase (PON) activities in patients with renal tumors .

Materials and methods

A total of 32 male patients with renal cell cancer with a mean age of 55.32 +2.9 were included in the study. All of the patients have not smoked during their life, they were not addicted to alcohol, have not used the supportive antioxidant, and did not abuse any drug and

have any metabolic disorders. There were no other major diseases or cancers in any of the patients except for the kidney tumor. All of the patients have been newly diagnosed, and their blood samples were received in the preoperative period. In all, 29 male patients who made up the control group (mean age 56.01 + 3.0) were randomly selected among the volunteers who did not have any known major disease and who did not use cigarettes, alcohol, drugs, and additional antioxidants. Patient and control groups had a similar socioeconomic status.

According to the results of radiological and postoperative histopathological evaluation, 24 (75%) of our patients were in stage 1, 6 (18.75%) of them were in stage 2, and 2 (6.25%) of them were in stage 4 of metastatic renal tumor.

The study protocol was carried out in accordance with the Helsinki Declaration as revised in 1989. All participants were informed about the study protocol and the written consent was taken from each one.

Blood collection;

Following 12 h of fasting period, blood samples were taken in the morning, collected into empty tubes, and immediately kept on ice at 4 °C. The serum was then isolated from the cells by centrifugation at 3000 rpm for 10 min. Serum samples for measurement of Nitric Oxide (NO), Arylesterase (ARE) and paraoxonase (PON) levels were kept at 20°C until they were used.

Methods of Analysis

Nitric Oxide (NO)

NO levels in serum was determined using the Griess reaction. Griess solution X: 0.1 g NED (N-1-naphthyl)-ethylenediamine dihydrochloride) was weighed and dissolved in 100 ml water. Again, Y Griess solution: 1 g sulphanilamide in 100 ml of orthophosphoric acid (5%) was dissolved in a solution. 100 mico liter sample was taken and each tube was placed in a 0.1 ml Griess solution X and 0.1 ml Griess solution Y equal to tubes placed in and stirred, then 15 minutes at room temperature was allowed to stand and each sample at 540 nm absorbance values ​​were read.

Arylesterase (ARE)

Arylesterase activity in 2004 and 2005, developed by Erel was determined with a kit. 10 μml onto 990 ml diluent solution was added 10/100 ratio dilutions were performed this diluted from the 3 μml enrolled over 260 μml pure water (Reagent 1) was added, then 10 μml Reagent 2 was added, then vortexed and at 548 nm enzyme activity was measured. Measurements are taken more spectrokuvet A1 80 μml Reagent 3 was added and again after waiting 4 minutes at 548 nm was measured and the measurements of activity is defined as A2. For activity measurement (enzyme unit) = (ΔA2-ΔA1) x1316.

Paraoxanase (PON)

Paraoxonase activity in 2004 and 2005, developed by Erel was determined with a kit. The two tubes are each 500 μml reagent 1 (buffer solution) was added and on 25 μml sample (serum) was added and stirred then 25 μml reagent 2 (substrate solution) was added 30 sec and 150 sec after the absorbance measurement at 412 nm was read. Activity measurement (U / L) = [(Δ150sn-Δ30sn) / 2] x1202.84

Statistical analysis

Descriptive statistics for the studied traits were expressed (reported) as mean, standard deviation, minimum, andÄ°statistiksel yorum maximum values. Student’s t test was used for comparison of groups. In the study, 5% level was taken into account to the statistically significant differences between groups, and SPSS Statistical package program (ver. 13) was used for the all statistical computations.

Results

The demographic and clinical data of bladder cancer and control groups are shown in Table 1. There were no statistically significant differences between renal cancer patients and controls with respect to age and body mass index (BMI) (all ps > 0.05; Table 1).

Serum NO level was significantly higher in renal cancer than in controls (all ps < 0.05); while ARE and PON levels were significantly lower (p < 0.05; Table 2). No correlation was observed between tumor staging and serum NO, ARE and PON levels (ps > 0.05).

Discussions

Biological and biochemical systems (CAT), peroxidase (POD), glutathione reductase (GSSG-Rx) and superoxide dismutase (SOD) are enzymes having antioxidant activity. Antioxidant defense system, cell free radical or other reactive molecules protects against oxidative damage. Therefore, this defense system, CAT, POD, PON, ARE, GSSG-Rx and antioxidant enzymes such as SOD is of great importance. The harmful effects of free radicals in cells are controlled by antioxidant defense systems.

Although some possible mechanisms through which oxidative stress exerts a regulatory role in tumor growth and progression including genomic instability, oncogene activation and angiogenesis are known, several important questions remain unanswered (12,13,14). It is not clearly known whether oxidative stres and tumor result from an increased oxidant production or from a failure of antioxidant systems (15). Although important changes in cellular redox homeostasis during tumor growth have been documented in experimental models, such variations have not been shown in humans. Most of the difficulties encountered in these studies are related to the complexity of the biochemical pathways that regulate the cellular redox balance (16,17). A wide variety of oxidizing molecules such as ROS and/or depleting agents can change the glutathione redox state, which is normally maintained by the activity of GSH depleting (GSH-Px) and replenishing enzymes (glutathione reductase). The importance of GSH and related enzymes and their variation in tumors has been poorly studied (16,13).

The enzymes eliminate oxygen free radicals of the cell plays an important role in the protection from oxidative damage. Antioxidant status and lipid peroxide and oxidized proteins well known marker of oxidative stress as measured by the relationship between the level and posture better reflects the health index. Cholesterol free radicals, arachidonic and deoksihegzanet binds to and initiates lipid peroxidation. One of the best indicators of this process has begun ROS can cause renal damage and cardiovascular disorders. In a study conducted in rats of cigarette smoke effects on antioxidant enzymes and lipid peroxidation has been studied, a significant increase in lipid peroxidation was observed that while no significant difference in antioxidant enzymes.

Abnormal cell proliferation in the serum cancerous patient is the cause of lipid peroxidation (LP) increase. The increase in LP in cancer may also be owing to the poor antioxidant system as observed in the previous studies (18). It has been claimed that MDA acts as a tumor promoter and cocarcinogenic agent on account of its high cytotoxicity and inhibitory action on protective enzymes (19,20). The data reported in the literature on MDA levels in different human cancer types are controversial. On the other hand, MDA, the major aldehyde end product of LP of membrane polyunsaturated fatty acids by free radicals, is an indicator of oxidative stress (21). In the present study, we found a significantly increased serum MDA levels in patients with renal cancer than in control subjects.

The data reported in the literature on oxidant, antioxidant molecule, and enzymes in different human cancer types are controversial. For instance, in a study the activities of SOD and GSH-Px enzymes were found lower in malignant liver tissues during rat hepatocarcinogenesis (22). In another one, Corrocher et al. established that in human hepatoma the enzymatic antioxidant system was severely impaired owing to lowered GSH-Px activities (23). Nakada et al. measured SOD activities in renal cell carcinoma and nontumorous renal tissues (24). They found no meaningful differences between the activities of the cancerous and noncancerous parts and suggested that it was unlikely for SOD to play a part in the development of renal cell carcinoma since SOD activities in tumor tissue were similar to those in nontumorous renal tissues (24). Ray et al. observed a significant increase in SOD and GSH-Px activities in patients with gastric cancer compare to the control group (8). Ozturk et al. observed a significant increase in xanthine oxidase (XO) activity in patients with cancerous human colorectal tissues compared to control group (25). The increased GSH-Px activities and GSH levels are reported in patients with leukemia (26,27).

NO levels in prostate cancer patients is increased compared to healthy humants . NO studies may be related to tumor growth by two separate mechanisms. First, the stimulation of angiogenesis, and the other pole of DNA by the activation of free radicals is increased mutagenesis. In addition, the release of NO from tumor cells, through non antiproliferative effects may follow from a role in tumor-induced immunosuppression . The present our study supports in literature studies.

The reduction of antioxidant enzyme activity increases as a result of oxidative DNA damage, has been found to be proportional . In addition, in the literature study in coronary artery disease oxidative DNA level has been found increased . In our study group, serum ARE was significantly lower than the control group (p <0.001).

Conclusions:

According to the results of our study of patients with renal cell carcinoma was found a decrease in the antioxidant defense system. Oxidant / antioxidant balance of damage in the development kidney cancer might be considered a risk factor. This is relevant for the formation of a konsessus randomized prospective studies are needed.

Parameters

Patients (n= 32)

Controls (n=29)

Age, year

55.32 ± 2.9

56.01 ± 3.0

Body mass index, kg/m2

21.56 ± 1.86

21.33 ± 1.29

Table 1. Demographic characteristics of the two groups in this study.

 

Patients (n=32)

(XSx)

Control

(n=29)

(XSx)

p

NO (µmol/L)

8.397± 2.0981

1.192± 0.1474

<0.001

ARE (U/mL)

17.518±3.5288

42.170± 6.8991

<0.001

PON (U/mL)

57.570±7.2911

94.423±4.7110

<0.001

Table 2. Descriptive statistics and comparison results according to the groups for specifications.

References:

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  2. Chow WH, Devesa SS, Warren JL et al. Rising incidence of renal cell cancer in the United States. JAMA. 1999; 281: 1628–31.
  3. Dhote R, Pellicer-Coeuret M, Thiounn N, et al. Risk factors for adult renal cell carcinoma: a systematic review and implications for prevention. BJU Int. 2000; 86: 20–7.
  4. McLaughlin JK, Blot WJ, Devesa SS et al. Renal cancer. In: Schottenfeld D and Fraumeni JF (eds) Cancer Epidemiology and Prevention. New York, NY: Oxford University Press, pp. 1996; 1142–55.
  5. Templar J, Kon SP, Milligan TP, et al. Increased plasma malondialdehyde levels in glomerular disease as determined by a fully validated HPLC method. Nephrology Dialysis Transplantation. 1999; 14: 946–51.
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  7. Nishikawa M. Reactive oxygen species in tumor metastasis. Cancer Lett. 2008; 266: 53–9.
  8. Ray G, Batra S, Shukla NK et al. Lipid peroxidation, free radical and antioxidant status in breast cancer. Breast Cancer Res Treat. 2000; 59:163–70.
  9. Wang GQ, Dawsey SM, Li Y. Effects of vitamin/ mineral supplementation on the prevalance of histological dysplasia and early cancer of the esophagus and stomach: results from the general population trial in Linxian, China. Cancer Epidemiology, Biomarkers and Prevention 1994; 3: 161–66.
  10. Oberley LW, Buettner GR. The role of superoxide dismutase in cancer: a review. Cancer Research. 1979; 39: 1141–9.
  11. Gecit I, Aslan M, Gunes M, et al. Serum prolidase activity, oxidative stress, and nitric oxidelevels in patients with bladder cancer. J Cancer Res Clin Oncol. 2012; 138: 739–43.
  12. Jaruga P, Zastawny TH, Skokowski J, et al. Oxidative DNA base damage and antioxidant enzyme activities in human lung cancer. FEBS Lett. 1994; 341(1):59-64.
  13. Sun Y, Oberley LW. Redox regulation of transcriptional activators. Free Radical Free Radic Biol Med. 1996; 21: 335–48.
  14. Blackburn RV, Spitz DR, Liu X, et al. Metabolic oxidative stress activates signal transduction and gene expression during glucose deprivation in human tumor cells. Free Radic Biol Med. 1999; 26: 419–30.
  15. Toyokuni S, Okamoto K, Yodoi J, et al. Persistent oxidative stress in cancer. FEBS Lett. 1995; 16: 3581–3.
  16. Mantovani G, MaccioA, Madeddu C, et al. Quantitative evaluation of oxidative stress, chronic inflammatory indices and leptin in cancer patients: correlation with stage and performance status. International Journal of Cancer. 2002; 98: 84–91.
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  18. Szatrowski TP, Nathan CF. Production of large amounts of H2O2 by human tumor cells. Cancer Res. 1991; 51: 794–8.
  19. Marnett LJ. Lipid peroxidation–DNA damage by malondialdehyde. Mutat Res. 1999; 424: 83–95.
  20. Seven A, Civelek S, Inci E, et al. Evaluation of oxidative stress parameters in blood of patients with laryngeal carcinoma. Clinical Biochemistry. 1999; 32: 369–73.
  21. Marnett LJ. Oxyradicals and DNA damage. Carcinogenesis. 2000; 21: 361–370.
  22. Vo TKO, Druez C, Delzenne N, et al. Analysis of antioxidant defence systems during rat hepatocarcinogenesis. Carcinogenesis. 1988; 9(11): 2009–2013.
  23. Corrocher R, Casaril M, Bellisola G, et al. Severe impairment of antioxidant system in human hepatoma. Cancer. 1986; 58(8): 1658–62.
  24. Nakada T, Akiya T, Koike H et al. Superoxide dismutase activity in renal cell carcinoma. Eur Urol. 1988; 14(1): 50–5.
  25. Ozturk HS, Karaayvaz M, Kacmaz M, et al. Activities of the enzymes participating in purine and free-radical metabolism in cancerous human colorectal tissues. Cancer Biochemistry Biophysics. 1998; 16: 157–168.
  26. Farber CM, Kanganis DN, Liebes LF, et al. Antioxidant enzymes in lymphocytes from normal subjects and patientswith chronic lymphocytic leukaemia: increased glutathione peroxidase activity in CLL B lymphocytes. Br J Haematol. 1989; 72: 32–5.
  27. Ferraris AM, Rolfo M, Mangerini R, et al. Increased glutathione in chronic lymphocytic leukemia lymphocytes. Am J Hematol. 1994; 47: 237–8.

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