Lead is an industrial pollutant that may exert specific toxic effects on male mammals. The aim of this study was to investigate further the protective effects of vitamin E on lead acetate (Pb)-induced reproductive toxicities and genotoxic effects on male rats. Sexually mature male Wistar rats (weighing 120-160 g) were given Pb (20 mg/Kg) and vitamin E (600 mg/kg/rat) orally for 20 days. The sperm count, sperm motility, sperm morphology, chromosomal aberrations, FSH, LH and testosterone levels, and histopathological changes in the testes of the rats were investigated after 20 days. Results revealed a statistically significant (p<0.01) increase in the number of abnormal sperm in treated animals. Lead acetate increased the percentage of chromosomal abnormalities. A significant decrease in LH, FSH and testosterone were observed in the treated group compared to the control. Pathological examination of testicular tissues showed degenerative changes of spermatogonia and spermatocytes to advanced degeneration and vacuolation. Lead acetate can be considered to have an environmental genotoxic and cytotoxic effect in the male rat and may contribute to a reduction of fertility. Vitamin E administration could reduce the genotoxic effect of lead in somatic and germ cells.
Pregnant rats received 0, 2% of lead acetate (Pb) in drinking water. The treatment with the aqueous extract of Pimpinella anisum L (P.A.E.) started after weaning with dose of 750 mg/kg and for 15 successive days. The effect of the extract was evaluated through behavioral tests : open filed (OF) , Forced swimming test (FST) and dark /light test. Beside; Lactate dehydrogenase (LDH), total plasmatic proteins, alkaline phosphatase (ALP), lipid peroxidation (TBARS) and Catalase (CAT) were analyzed. Lead induced a hyperactivity in the open field which was reduced after administration of P.A.E. In the FST, the treatment with plant extract enhanced significantly the mobility time compared with intoxicated group. We had observed that time spent in the dark compartments in dark and light test was reduced after oral administration of P.A.E. Lead caused significant increase in LDH , TBARS and ALP , in contrary this toxic agent decrease the levels of plasmatic proteins and catalase activity in cerebellum and cerebrum. We can conclude that oral treatment with aniseed aqueous extract was effective in reducing the level of some of biochemical parameters and ameliorate behavior of intoxicated rats by lead.
Environmental exposure to toxic levels of lead (Pb) occurs in a number of industries with potential adverse effects on the reproductive capacity of exposed men. Clinical and animal studies indicate that abnormalities of spermatogenesis result from toxic lead exposure, but eventual histopathologic alterations involved have not been identified. To explore putative abnormalities in the reproductive gonadotropic axis following lead intoxication, experimental animals when exposed to low levels of lead, 65 days old animals were treated with distilled water containing 0,0 mg (control), 10 mg lead (Pb)/Kg/day and 15 mg lead (Pb)/Kg/day intraperitoneally for 20 days. At the end of treatment, the animals were sacrificed and the blood collected for luteinizing hormone (LH) and testosterone assays. The testis was processed for histological analysis. The results showed a high serum concentration of LH and testosterone in lead-treated animals compared to controls. Histological examination of testis showed deformities in testicular morphology of lead intoxicated animals with gross damage within the somniferous tubules. A strong correlation was established between LH and testosterone suggesting an alteration in the endocrine components of the gonadotropic axis. Histological examination of pituitary gland showed some degenerative changes in endocrine cells of lead group. Changes in LH and testosterone levels suggest that Pb exposure during the critical time of sexual differentiation induces reproductive axis abnormalities in adulthood. In conclusion, lead has a gonadotoxic effect by decreasing LH and testosterone levels and damaging the testis seminiferous tubules. Catalase activity was significantly reduced in the lead group following 65 days of exposure which possibly indicates that lead might had other mechanisms of action, such as increasing oxidative damage.
Previous human and experimental studies have demonstrated that lead exposure may modify the metabolism of lipid. Oxidative stress with subsequent lipid peroxidation has been postulated as one mechanism for lead toxicity. The protective action of vitamins C against lead affects lipid hydroperoxide level and liver functions in male rats has been studied. Experiments were performed on male waster rats with body weights of 120-160 g. Male wistar rats were exposed to 3 g/l lead acetate in drinking water for 5 weeks and treated thereafter with vitamin C (500 mg/kg, orally) for 28 days. One day after the feeding was over, venous blood samples, under chloroform anesthesia, were collected. The animals were killed by exsanguinations and the liver was excise for determination the metal content and histopathological changes. Similarly, the tissue lipid (lipid peroxidation) and the enzyme fraction (superoxide dismutase (SOD), catalase (CAT), alkaline phosphatase (ALP), acid phosphatase (ACP) and glutathione (GSH) were also measured in the liver. Metal content in blood and liver was determined by means of atomic absorption spectrophotometry. Administration of lead acetate (3 g/l) in drinking water for 5 weeks induced a significant increase in the levels of hepatic ALP, ACP and lipid peroxidation. Lead acetate exposure also produced detrimental effects on the redox status of the liver indicated by a significant decline in the levels of liver antioxidants such SOD, CAT and GSH. Further, there was a significant increase in the levels of lead in blood and liver of animals exposed to lead. However, oral administration of vitamin C at dose level of 500 mg/kg body weight reduced the alterations in the previous parameters. Histological examination of the liver also revealed pathophysiological changes in lead acetate-exposed group and treatment with vitamin C improved liver histology. The result of this study strongly indicate that vitamin C has got a potent antioxidant action against lead acetate induced hepatic damage in rats.
Many heavy metals and metalloids (e.g., Pb, Cd, and Ni) can contaminate the environment and cause severe health problems. Through this study, investigated the possible corrective effects of Ficus carica extract (FCE) against nickel (Ni) induced stress response and damage on the liver of rats. Male Wistar rats were divided into four groups (8 rats per group) and co-treated with FCE (350 mg/kg) and exposed to Nickel chloride (10 mg/kg) for 4-weeks. The volatile compounds of FCE were characterized by solid phase micro-extraction (SPME) coupled with GC-MS, and the biochemical parameters of stress were determined. The SPME-GC/MS analysis of FCE indicated the presence of thirty (30) phyto-bioactive compounds including alcohols, aldehydes, organic acids, ketones, furans, terpenes, ester and others. The best capacity for scavenging DPPH free radicals and metal chelating were found with the IC 50 values of 0.49 and 2.91 mg/mL, respectively. Ni induced damage to various macromolecules. Malondialdehyde, protein carbonyls, alanine aminotransferase and gamma glutamyl transferarse levels were significantly increased in Ni exposed group compared to control group and co-treatment with FCE reduced the levels of these parameters. In conclusion, current findings showed that Ni-induced oxidative damage and the administration of FCE can improve correct and restore the alteration in the rat liver.
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