Testicular toxicity in mercuric chloride treated rats: association with oxidative stress.

Mercury has been recognized as an industrial hazard that adversely affects male reproductive systems of humans and animals. However, less information is available concerning the underlying mechanism in the pathogenesis of male reproductive dysfunction. The present study investigated the possible involvement of oxidative stress to induce oxidative deterioration of testicular functions in adult rats. Wistar male rats (n=132) were continuously exposed to HgCl(2) at 0, 50 and 100 ppm during 90 days through oral administration in the drinking water. Mercury exposure for 90 days resulted in an increase in the absolute and relative wet weight of the testis and a decrease in the absolute and relative wet weight of the accessory sex glands, with respect to the matched control. Marked perturbation in testosterone serum level was also detected during the treatment for the treated groups. Cauda epididymal sperm count/motility decreased significantly in the mercury-treated group and qualitative examination of testicular sections revealed a fewer mature luminal spermatozoa in comparison to the control. When the mercury-treated males were mated with normal cyclic females, mercury exposure resulted in a decline of the reproductive performance of male rats. These effects were associated with a significant increase in mercury content of testes and blood in time-dependent and dose-dependent fashion, respectively. The HgCl(2) treatment was associated with oxidative stress. Evidence of induction of oxidative stress was obtained in terms of perturbations in antioxidant defense and a significant dose-dependent increase in the testicular lipid peroxidation as a consequence of pro-oxidant exposure. Taken together, the results suggest that an increase in free radical formation relative to loss of antioxidant defense system after mercury exposure may render testis more susceptible to oxidative damage leading to their functional inactivation.

[Impact of green tea on oxidative stress induced by ammonium metavanadate exposure in male rats]. / Impact du thé vert sur l'effet oxydatif du métavanadate d'ammonium chez le rat male pubère.

Transitional metals, as vanadium, are known to exert noxious effects by generating oxidative stress. Addition of antioxidants in the diet could decrease the cytotoxic effect related to the oxidative stress. The present study, carried out in Wistar rats, is a contribution to the evaluation of protective effects of green tea Camellia sinensis, which is known to be rich in antioxidant compounds (polyphenols...). Rats were divided into four groups: (C) was control, (V) was given ammonium metavanadate (AMV), (TH) was given herbal tea as drink (66 g/l) and TH + V was given tea and metavanadate. Group (TH) was given herbal tea one month before vanadium treatment. Metavanadate was daily i.p. injected (5 mg NH4VO3/kg body weight) for 10 days. (C) and (TH) groups received i.p. injections of 0.9% NaCl during the same period. Changes in lipid peroxidation levels (TBARS) in kidney, liver and testes, serum concentrations of vitamins E and A and superoxidismutase (SOD) and catalase (CAT) activities in blood cells were determined. One month pre-treatment with green tea, followed by 10 days of treatment (TH) did not change TBARS in liver and testes as compared to controls, but induced a clear decrease of TBARS in kidneys. Intraperitoneal administration of AMV to rats (V) induced a time-dependant increase of TBARS in kidney, liver and testes that was lowered in rats (V + TH) drinking tea. Vitamin E concentrations were found to be drastically decreased from day 1 to 10 in rats (V). Vitamin A concentration was decreased at day 10 only. Drinking tea lowered AMV inhibitory effects in rats (V + TH), and conversely an increase of vitamins A and E concentrations were found at day 10. SOD and catalase activities were found increased in the blood cells from day 1 to day 5 and conversely decreased at day 10. In contrast, associated to green tea, AMV did not affect SOD and catalase activities compared to controls.

[Interaction of intermittent fasting on the cytotoxic effects of nickel in rats at puberty]. / Interaction du jeûne intermittent sur les effets cytotoxiques rénaux du nickel chez le rat pubère.

This study has been undertaken with the aim of determining if intermittent fasting can be considered as a malnutrition that amplifies, according to numerous authors, the cytotoxic effects of environmental pollutants. We have used 200 male and female rats of 'Wistar' descent (BW approximately 180 g). These rats are distributed into two groups: some nourished daily (N) and others nourished one day over two (J) during a month. By the end of this month, each group is itself split into two subgroups, the first one receiving tap water as drinkable water (group NO and JO); the other one receiving the water enriched by the chloride of nickel at the rate of 100 mg NiCl2 per litre (groups NNi and JNi). Intermittent fasting goes on parallel to treatment during 2, 4, 10, 16, 30 and 60 days. For the exploration of the protein of stress (HSP) and of the metallothioneines (MT), the nickel is administered by injection at the rate of 4 mg NiCl2 per kg during 1 and 5 days. Our results show that the mineral seric and renal balance does not vary in conditions of intermittent fasting compared with conditions of normal nutrition. Our study show than that nickel induced a renal deficiency by decreasing the creatinemia and uraemia rate, which is confirmed by the histological study, and induced a decrease in the induction of the HSP73 and in the synthesis of the (MT). The association of nickel with intermittent fasting would inhibit these effects. In conclusion, intermittent fasting does not manifest itself as a malnutrition that amplifies the nickel's effects. Nevertheless, it seems that the calorific lack provoked by intermittent fasting is beneficial to the body by increasing its performances against the cytotoxic effects induced by nickel.