Hanen Bouaziz

Antioxidant effect of vitamin E and selenium on hepatotoxicity induced by dimethoate in female adult rats

Acute exposure to pesticides can cause hepatotoxicity. Our study pertains to the potential ability of selenium and/or vitamin E, used as nutritional supplements, to alleviate oxidative stress induced by dimethoate. Female Wistar rats were randomly divided into seven groups of six each: group I served as controls; group II received in their drinking water dimethoate (2 g L(-1)); group III received both dimethoate and selenium (0.5 mg/kg of diet); group IV was treated with dimethoate and vitamin E (100 mg/kg of diet); group V received dimethoate+selenium+vitamin E and groups VI and VII received either selenium or vitamin E. The exposure of rats to dimethoate for 30 days promoted oxidative stress with an increase in malondialdehyde and a decrease in glutathione and non-protein thiol levels. A decrease in glutathione peroxidase, superoxide dismutase and catalase activities was also observed. While, plasma transaminases, lactate dehydrogenase activities and bilirubin levels increased. Co-administration of selenium and/or vitamin E through diet improved the biochemical parameters cited above. Liver histological studies confirmed biochemical parameters and the beneficial roles of selenium and vitamin E.

Cardioprotective effects of selenium on chromium (VI)-induced toxicity in female rats.

Acute exposure to hexavalent chromium compounds can cause cardiotoxicity. Our study pertains to the protective effect of selenium against K(2)Cr(2)O(7)-induced cardiotoxicity. Female Wistar rats were divided into four groups of six each: group I served as controls which received standard diet; group II received in drinking water K(2)Cr(2)O(7) alone (700 ppm); group III received both K(2)Cr(2)O(7) and Se (0.5 Na(2)SeO(3) mg/kg of diet); group IV received Se (0.5 mg/kg of diet) for 3 weeks. The exposure of rats to chromium promoted oxidative stress with an increase in malondialdehyde levels and a decrease in antioxidant non-enzymatic levels such as glutathione, non-protein thiol and vitamin C, while, an increase in glutathione peroxidase, superoxide dismutase and catalase activities was observed. However, plasma transaminases, lactate dehydrogenase activities, cholesterol, triglycerides and low density lipoprotein-cholesterol levels increased, and high density lipoprotein-cholesterol decreased. Coadministration of Se restored the parameters cited above to near-normal values. The histopathological findings confirmed the biochemical results.

Dimethoate-induced oxidative damage in erythrocytes of female adult rats: possible protective effect of vitamin E and selenium supplemented to diet

Pesticide hazards have been accentuated by the sharp rise in their agricultural, industrial and domestic use. Acute exposure to pesticides can cause oxidative damage. Our study investigated the potential ability of selenium (Se) and/or vitamin E, used as nutritional supplements, to alleviate erythrocyte oxidative damage induced by dimethoate (DM), an organophosphate pesticide. Female Wistar rats were exposed to DM (0.2g/L−1 of drinking water), DM + Se (0.5 mg/kg of diet), DM + vitamin E (100 mg/kg of diet), or DM + Se + vitamin E. Rats exposed to DM for 30 days showed an increase in malondialdehyde levels, superoxide dismutase and glutathione peroxidase activities in their erythocytes, while Na+,K+-ATPase and catalase activities, glutathione, non-protein thiol, vitamin E and vitamin C levels decreased. We also noted an increase in lactate dehydrogenase activity, marker of haemolysis and a decrease in acetylcholinesterase, the principal mode of organophosphorus action. Co-administration of Se or vitamin E to the diet of DM-treated rats ameliorated the biochemical parameters cited above. But the combined effect of Se and vitamin E was more powerful in antagonizing DM-induced oxidative stress. Therefore, our investigation revealed that both Se and vitamin E were useful elements in preventing DM-induced erythrocytes damage.

Neurotoxicity and oxidative stress induced by gibberellic acid in rats during late pregnancy and early postnatal periods: Biochemical and histological changes

Gibberellic acid (GA(3)) is an endogenous plant growth regulator used worldwide in agriculture; however, little is known about its biochemical and physiological effects on mammals. This study investigated possible neurotoxic effects of GA(3) on the cerebrum and cerebellum of suckling rats. Female Wistar rats were given daily 200 ppm GA(3) in drinking water from the 14th day of pregnancy until day 14 after delivery. Acetylcholinesterase activity in both cerebellum and cerebrum was inhibited after treatment with GA(3). Neurotoxicity was demonstrated by a significant increase in malondialdehyde level and a decrease in the antioxidant enzyme activities of catalase, superoxide dismutase, glutathione peroxidase in the cerebrum and cerebellum of suckling pups. A significant decline of glutathione content and vitamin C was also observed. The biochemical parameters were correlated histologically with an abnormal development of the external granular layer and a loss of Purkinje cells in the cerebellum of GA(3)-treated suckling rats.

Oxidative stress induced by chromium (VI) in bone of suckling rats

Exposure to hexavalent chromium Cr(VI) compounds is of concern in many Cr-related industries and their surrounding environments. K2Cr2O7 is widely recognized as an animal and human carcinogen, mutagen, and teratogen. The present study investigated the bone maturity of suckling rats whose mothers were treated with K2Cr2O7. Experiments were carried out on female Wistar rats given 700 ppm of K2Cr2O7 in their drinking water from the 14th day of pregnancy until day 14 after delivery. Exposing dams to K2Cr2O7 caused disorders in the bone of their progeny. As corollary to this, malondialdehyde levels increased, while glutathione, a non-protein thiol and vitamin C decreased. Alteration of the antioxidant system in the treated group was also confirmed by the significant decline of superoxide dismutase, catalase, and glutathione peroxidase activities. Furthermore, K2Cr2O7 induced changes in bone mineralization, especially calcium and phosphorus levels, which decreased. Whereas, in plasma and urine, they increased and decreased inversely. These results suggest that K2Cr2O7 accelerated bone resorption activity. In fact, in treated pups, total tartrate-resistant acid phosphatase, which reflected bone resorption, was enhanced while total alkaline phosphatase, which reflected bone formation, was reduced. The impairment of bone function was corresponded histologically.

Nephrotoxicity induced by chromium (VI) in adult rats and their progeny

To assess kidney damages in pregnant and lactating rats and in their suckling pups, Wistar female rats were given, through drinking water, 700 parts per million (ppm) of K2Cr2O7 from the 14th day of pregnancy until day 14 after delivery. Toxicity was objectified by a significant increase in malondialdehyde (MDA), glutathione (GSH) and nitric oxide (NO) levels in kidney of chromium-treated mothers and their suckling pups. Moreover, lactate dehydrogenase (LDH) was increased in kidney and decreased in plasma of K2Cr2O7-treated rats. Activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were increased in dams and decreased in their pups. Interestingly, these biochemical modifications were accompanied by higher plasma and lower urinary levels of creatinine, a specific indicator of glomerular function, and of urea than those of controls. Significant increase in creatinine clearance was also found in treated mothers and in their progeny. Histological studies showed an infiltration of mononuclear cells, necrosis and vascular congestion in kidney of pups and dams. Based on the present findings, K2Cr2O7 administrated to female rats during late pregnancy and early postnatal periods provoked kidney damages in dams and their offspring.

Toxic effects of chromium (VI) by maternal ingestion on liver function of female rats and their suckling pups

Potassium dichromate (K2Cr2O7) is an environmental contaminant widely recognized as a carcinogen, mutagen, and teratogen toward humans and animals. This study investigated the effects of K2Cr2O7 on the hepatic function of pregnant and lactating rats and their suckling pups. Experiments were carried out on female Wistar rats given 700 ppm of K2Cr2O7 in their drinking water from the 14th day of pregnancy until day 14 after delivery. Hepatotoxicity was objectified by the significant increase in liver malondialdehyde content and a significant accumulation of chromium in this soft tissue. Moreover, exposure to K2Cr2O7 induced a decrease of glutathione, nonprotein thiols, and vitamin C in the liver of mothers and their suckling pups. Alteration of the antioxidant system in the treated group was confirmed by the significant decline of antioxidant enzyme activities such as catalase, glutathione peroxidase, while liver superoxide dismutase activity increased in mothers and decreased in their offspring. It was found that K2Cr2O7 induced liver damages as evidenced by the elevation of plasma aminotransferases, lactate dehydrogenase activities, and bilirubin levels. Impairment of the hepatic function corresponded histologically. Our investigation revealed hemorrhage, leukocytes infiltration cells, and necrosis, which were more pronounced in the hepatocytes of mothers than in those of their suckling pups.

Oxidative stress induced by gibberellic acid in bone of suckling rats.

The present study investigates the bone maturity of suckling rats whose mothers were treated with gibberellic acid (GA(3)). Female Wistar rats were divided into two groups: group I that served as controls and group II that received orally GA(3) (200 ppm) from the 14th day of pregnancy until day 14 after delivery. In the GA(3) group, an increase in body and femur weights as well as in femur length of pups was noted when compared to controls. Lipid peroxidation was demonstrated by high femur malondialdehyde levels, while superoxide dismutase, catalase, glutathione peroxidase activities, glutathione and vitamin C levels in femur decreased. GA(3) caused a decrease in calcium and phosphorus levels in bone. The calcium concentration in plasma increased and the phosphorus concentration decreased, while urinary levels of calcium decreased and those of phosphate increased. Moreover, plasma total tartrate-resistant acid phosphatase and total alkaline phosphatase increased. Bone disorders were confirmed by femur histological changes.

Oxidative damage in erythrocytes of adult rats and their suckling pups exposed to gibberellic acid

Gibberellic acid (GA3) is a plant growth regulator used in agriculture worldwide. The present study investigated the propensity of GA3 to induce hematological disorders. Pregnant Wistar rats were randomly divided into two groups: group I served as controls; group II received orally GA3 (200 ppm) from the 14th day of pregnancy until day 14 after delivery. GA3 reduced the number of red blood cells, hemoglobin concentration, and hematocrit in suckling rats, while these parameters remained unchanged in their mothers. White blood cells increased in mothers and were unchanged in their pups. Several studies have associated these hematological disorders with oxidative stress. In fact, GA3 treatment revealed in erythrocytes a significant increase in malondialdehyde levels and a decrease in antioxidant enzyme activities such as superoxide dismutase, catalase, and glutathione peroxidase. Moreover, a significant decline was observed in acetylcholinesterase activity, glutathione, nonprotein thiols, and vitamin C levels.

Effect of selenium on hypothyroidism induced by methimazole (MMI) in lactating rats and their pups

The present study was undertaken to assess the effect of selenium (Se) on hypothyroidism induced by methimazole (MMI) in lactating rats and their pups. Rats were randomly divided into four groups of six each: group I served as a negative control which received standard diet; group II received orally MMI (250 mg L -1 ); group II received both MMI (250 mg L -1 , orally) and Se (0.5 mg/kg of diet); group IV served as a positive control and received Se (0.5 mg Na 2 SeO 3 /kg of diet). Treatments were started from the 14th day of pregnancy until postnatal day 14. In the MMI-exposed group, the body weight of 14-day-old pups diminished compared to controls; besides, a hypertrophy of the thyroid glands was observed. Co-administration of Se through the diet restored these parameters to near normal values. In the MMI-treated group, thyroid iodine contents and plasma thyroid hormone levels significantly decreased, while plasma TSH levels increased in pups and their mothers. These biochemical modifications corresponded histologically to closed follicles, increased vascularity and a reduction in colloid volume. Co-treatment with Se ameliorated these parameters. We concluded that the supplementation of Se in diet had beneficial effects on hypothyroidism during a critical period of life.