Suna Kalender

Malathion-induced testicular toxicity in male rats and the protective effect of vitamins C and E

Sexually mature male Wistar rats (weighing 300-320 g and each group 6 animals) were given malathion (27 mg/kg; 1/50 of the LD(50) for an oral dose) and/or vitamin C (200mg/kg)+vitamin E (200mg/kg) daily via gavage for 4 weeks. The sperm counts, sperm motility, sperm morphology, FSH, LH, and testosterone levels, and histopathological changes in the testes of these rats, were investigated at the end of the 4th week. By the end of 4th week, rats given malathion alone, or in combination with vitamins C and E, had significantly lower sperm counts and sperm motility, and significantly higher abnormal sperm numbers, than the untreated control rats. The rats given malathion alone or in combination with vitamins also had significantly lower plasma FSH, LH and testosterone levels than the control rats. Co-treatment of malathion-exposed rats with vitamins E and C had a protective effect on sperm counts, sperm motility and abnormal sperm numbers, but not on plasma FSH, LH and testosterone levels. Light microscopic investigations revealed that 4 weeks of malathion exposure was associated with necrosis and edema in the seminiferous tubules and interstitial tissues. Degenerative changes in the seminiferous tubules were also observed in the rats which received malathion and supplemented with vitamins C and E, but milder histopathological changes were observed in the interstitial tissues. Thus, it appears that vitamins C and E ameliorate malathion testicular toxicity but are not completely protective.

Effects of diazinon on pseudocholinesterase activity and haematological indices in rats: The protective role of Vitamin E.

Diazinon (DZN) is an organophosphate insecticide has been used in agriculture and domestic for several years. Vitamin E (200mg/kg, twice a week), diazinon (10mg/kg, per day) and Vitamin E (200mg/kg, twice a week)+diazinon (10mg/kg, per day) combination were given to rats orally via gavage for 7 weeks. Pseudocholinesterase in serum and haematological indices were investigated at the end of the 1st, 4th and 7th weeks comparatively with control group. At the end of 1st, 4th and 7th weeks, statistically significant decrease of pseudocholinesterase activity in serum were detected when diazinon- and Vitamin E+diazinon-treated groups compared to control group. When diazinon- and Vitamin E+diazinon-treated groups were compared to each other there were no significant changes. When diazinon-treated group was compared to control group, body weight decreased significantly at the end of the 4th and 7th weeks. It was observed that at the end of 1st, 4th and 7th weeks, there was a statistically significance in haematological indices except mean corpuscular hemoglobin (MCH) when diazinon-treated group was compared to control group. At the end of 1st week increase of thrombocyte, at the end of the 4th week increase of hemoglobin and thrombocyte and at the end of the 7th week increase of red blood cell (RBC), hemoglobin, hematocrit, mean corpuscular hemoglobin concentration (MCHC) and thrombocyte were observed statistically significant when Vitamin E+diazinon treated group was compared with diazinon treated group. According to the present study, we conclude that Vitamin E reduces diazinon toxicity, but it does not protect completely.

Malathion-induced hepatotoxicity in rats: the effects of vitamins C and E.

Mature male Wistar rats (weighing 300-320 g and each group six animals) were given malathion (27 mg/kg; 1/50 of the LD50 for an oral dose), vitamin C (200 mg/kg)+vitamin E (200 mg/kg), or both daily via gavage for 4 weeks. At the end of the fourth week, the malathion-treated group and the malathion plus vitamin-treated group both had significantly higher white blood cell (WBC) and thrombocyte counts than the control group. Compared to the control group, the two groups also had significantly higher serum total cholesterol, alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) levels, and significantly lower triglyceride and very low density lipoprotein (VLDL) levels. The malathion-treated rats also had significantly lower serum total protein and albumin levels, but the malathion plus vitamin-treated group did not differ from the control group in terms of these parameters. Moreover, concomitant vitamin treatment significantly normalized, at least partially, all of the other hematological and biochemical parameters that were altered by malathion. Light microscopic analyses revealed that both the malathion-treated and malathion plus vitamin-treated groups exhibited histopathological changes in liver tissues, although some pathological features were only observed in the malathion-treated group. Thus, vitamins C and E can reduce malathion hepatotoxicity, although the degree of protection they provide is limited.

Malathion-induced oxidative stress in human erythrocytes and the protective effect of vitamins C and E in vitro.

Malathion is an organophosphate (OP) pesticide that has been shown to induce oxidative stress in erythrocytes through the generation of free radicals and alteration of the cellular antioxidant defense system. We examined the effect of several different doses of malathion (25, 75, 200 μM), or malathion in combination with vitamin C (VC; 10 μM) or vitamin E (VE; 30 μM), on the levels of malondialdehyde (MDA), and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities in human erythrocytes in vitro. Erythrocytes were incubated under various treatment conditions (malathion alone, vitamins alone, or malathion plus vitamin) at 37°C for 60 min, and the levels of MDA, and SOD, CAT and GPx activities, were determined. Treatment with malathion alone increased the levels of MDA and decreased SOD, CAT, and GPx activities in erythrocytes (P < 0.05). There were no statistical differences among VC‐treated, VE‐treated, or VC + VE‐treated erythrocyes, as compared with nontreated control cells. Treatment of cells with malathion + VC, malathion + VE, or a combination of all three agents prevented malathion‐induced changes in antioxidant enzyme activity and lipid peroxidation. However, this effect was seen only at low concentrations of malathion (25 and 75 μM), and the combination of VC + VE had a more protective effect than VC or VE alone. These results indicated that the presence of vitamins at concentrations that are similar to the levels found in plasma have no effect on malathion‐induced toxicity in erythrocytes at a concentration of malathion (200 μM) that is typically used in pesticides.

Protective effect of catechin and quercetin on chlorpyrifos-induced lung toxicity in male rats.

The mature male Wistar rats (n=36, 300-320 g) were divided into six groups having six animals, i.e., Group I (control), Group II (catechin, 20 mg/kg bw), Group III (quercetin, 20 mg/kg bw), Group IV (chlorpyrifos 5.4 mg/kg, 1/25 LD50), Group V (catechin+chlorpyrifos) and Group VI (quercetin+chlorpyrifos). Rats were given chlorpyrifos, catechin and quercetin daily via gavage for 4 weeks. Chlorpyrifos increased the levels of malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT), and decreased glutathione peroxidase (GPx) and glutathione-S-transferase (GST) activities in lung tissues compared to the control group. In the catechin plus chlorpyrifos- and quercetin plus chlorpyrifos-treated groups, there were statistically significant increases in CAT and SOD activities, while no statistically significant changes were observed in MDA, GST and GPx activities relative to the control. Compared to the chlorpyrifos-treated group, however, the catechin plus chlorpyrifos- and quercetin plus chlorpyrifos-treated groups showed significantly increased GST and GPx activity, while the activity of MDA, SOD and CAT was significantly decreased. Light microscopic investigations revealed that 4 weeks of chlorpyrifos exposure induced numerous histopathological alterations in the lung. Milder histopathological changes were observed in animals co-treated with catechin plus chlorpyrifos or quercetin plus chlorpyrifos. Thus, it appears that catechin and quercetin ameliorate chlorpyrifos-induced lung toxicity but are not completely protective.

Mercuric chloride-induced testicular toxicity in rats and the protective role of sodium selenite and vitamin E

Mercury has been recognized as an environmental pollutant that adversely affects male reproductive systems of animals. This study examined the effects of mercuric chloride on the antioxidant system and histopathological changes and also evaluated the ameliorating effects of sodium selenite and/or vitamin E in the rat testis tissues. Sexually mature male Wistar rats (weighing 300-320g and each group six animals) were given mercuric chloride (1mg/kg bw) and/or sodium selenite (0.25mg/kg bw)+vitamin E (100mg/kg) daily via gavage for 4weeks. In the present study, mercuric chloride exposure resulted in an increase in the TBARS level and a decrease in the SOD, CAT, GPx activities, with respect to the control. Further, light microscopic investigation revealed that mercury exposure induced histopathological alterations in the testis tissues. Supplementation of sodium selenite and/or vitamin E to mercury-induced groups declined lipid peroxidation, increased SOD, CAT, GPx activities. While some histopathological changes were detected in mercuric chloride treated group, milder histopathological changes were observed in animal co-treated with sodium selenite and/or vitamin E supplementation to mercuric chloride-treated rats. As a result, mercuric chloride induced testicular toxicity is reduced by sodium selenite and/or vitamin E, but not ameliorate completely.

Protective role of antioxidant vitamin E and catechin on idarubicin-induced cardiotoxicity in rats

Idarubicin is an anthracycline antibiotic extensively used in acute leukemia. In the present study we investigated whether vitamin E and catechin can reduce the toxic effects of idarubicin. Vitamin E (200 IU kg(-1) week(-1)), catechin (200 mg kg(-1) week(-1)), idarubicin (5 mg kg(-1) week(-1)), idarubicin + vitamin E (200 IU kg(-1) week(-1)), and idarubicin + catechin (200 mg kg(-1) week(-1)) combinations were given to male Sprague-Dawley rats weighing 210 to 230 g (N = 6/group). Idarubicin-treated animals exhibited a decrease in body and heart weight, a decrease in myocardial contractility, and changes in ECG parameters (P<0.01). Catechin + idarubicin- and vitamin E + idarubicin-treated groups exhibited similar alterations, but changes were attenuated in comparison to those in cardiac muscle of idarubicin-treated rats (P<0.05). Superoxide dismutase and catalase activity was reduced in the idarubicin-treated group (P<0.05). Glutathione peroxidase levels were decreased in the idarubicin-treated group (P<0.05) and reached maximum concentrations in the catechin- and catechin + idarubicin-treated groups compared to control (P<0.01). Malondialdehyde activity was decreased in the catechin + idarubicin-treated groups compared to control and increased in the other groups, reaching maximum concentrations in the vitamin E-treated group (P<0.01). In electron microscopy studies, swelling of the mitochondria and dilatation of the sarcoplasmic reticulum of myocytes were observed in the idarubicin-treated groups. In groups that were given idarubicin + vitamin E and idarubicin + catechin, the only morphological change was a weak dilatation of the sarcoplasmic reticulum. We conclude that catechin and vitamin E significantly reduce idarubicin-induced cardiotoxicity in rats.

Sodium selenite and vitamin E in preventing mercuric chloride induced renal toxicity in rats

This study aims to investigate improving effects of sodium selenite and/or vitamin E on mercuric chloride-induced kidney impairments in rats. Wistar male rats were exposed either to sodium selenite (0.25mg/kgday), vitamin E (100mg/kgday), sodium selenite+vitamin E, mercuric chloride (1mg/kgday), sodium selenite+mercuric chloride, vitamin E+mercuric chloride and sodium selenite+vitamin E+mercuric chloride for 4weeks. Mercuric chloride exposure resulted in an increase in the uric acid, creatinine, blood urea nitrogen and malondialdehyde (MDA) levels and a decrease in the superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities. Histopathological changes were detected in kidney tissues in mercuric chloride-treated groups. A significant decrease in the uric acid, creatinine, blood urea nitrogen and MDA levels and a significant increase in the SOD, CAT and GPx activities were observed in the supplementation of sodium selenite and/or vitamin E to mercuric chloride-treated groups. Conclusively, sodium selenite, vitamin E and vitamin E+sodium selenite significantly reduce mercuric chloride induced nephrotoxicity in rats, but not protect completely.

Subacute effects of low dose lead nitrate and mercury chloride exposure on kidney of rats

Lead nitrate and mercury chloride are the most common heavy metal pollutants. In the present study, the effects of lead and mercury induced nephrotoxicity were studied in Wistar rats. Lead nitrate (LN, 45 mg/kg b.w/day) and mercury chloride (MC, 0.02 mg/kg b.w/day) and their combination were administered orally for 28 days. Four groups of rats were used in the study: control, LN, MC and LN plus MC groups. Serum biochemical parameters, lipid peroxidation, antioxidant enzymes and histopathological changes in kidney tissues were investigated in all treatment groups. LN and MC caused severe histopathological changes. It was shown that LN, MC and also co-treatment with LN and MC exposure induced significant increase in serum urea, uric acid and creatinine levels. There were also statistically significant changes in antioxidant enzyme activities (SOD, CAT, GPx and GST) and lipid peroxidation (MDA) in all groups except control group. In this study, we showed that MC caused more harmful effects than LN in rats.

Effects of lead nitrate and sodium selenite on DNA damage and oxidative stress in diabetic and non-diabetic rat erythrocytes and leucocytes

The adverse effects of lead nitrate (LN) and the preventive role of sodium selenite were investigated in diabetic and non-diabetic rat blood by measuring trolox equivalent antioxidant capacity (TEAC), ferric reducing antioxidant power (FRAP), malondialdehyde (MDA) levels and activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) also by evaluating DNA damage with comet assay. LN increased the levels of MDA, tail DNA%, mean tail length and tail moment, decreased the enzymes activities, FRAP and TEAC values. In sodium selenite+LN group, we observed the protective effect of sodium selenite on examining parameters. Diabetes caused alterations on these parameters, too. We found that sodium selenite did not protect against diabetes caused damages. As a result, LN caused toxic effects on blood cells and sodium selenite alleviated this toxicity but it did not show preventive effect against diabetes. Also, LN caused more harmfull effects in diabetic groups than non-diabetic groups.