ABSTRACT
Sodium fluoride (NaF), a widespread natural pollutant was given to sperm-positive female rats throughout gestation and lactation at a dose of 4.5 and 9.0 ppm via drinking water. The neonates were allowed to grow up to 90 days on tap water, and then sperm parameters, testicular steroidogenic marker enzyme activity levels, and circulatory hormone levels were studied. The sperm count, sperm motility, sperm coiling (hypoosmotic swelling test), and sperm viability were decreased in experimental rats when compared with controls. The activity levels of testicular steroidogenic marker enzymes (3beta hydroxysteroid dehydrogenase and 17beta hydroxysteroid dehydrogenase) were significantly decreased in experimental animals indicating decreased steroidogenesis. The serum testosterone, follicle stimulating hormone and luteinizing hormone levels were also significantly altered in experimental animals. Our data indicate that exposure to NaF during gestation and lactation affects male reproduction in adult rats by decreasing spermatogenesis and steroidogenesis.
Subject(s)
Reproduction/drug effects , Sexual Behavior, Animal/drug effects , Sodium Fluoride/toxicity , Sperm Count , Animals , Male , Rats , Spermatozoa/drug effects , Spermatozoa/physiologyABSTRACT
AIM: To investigate the effect of in utero exposure to hydroxyprogesterone (HP) on liver metabolism in adult male albino rats. METHODS: Pregnant Wistar strain albino rats were exposed to supra-normal levels (10 mg/kg and 25 mg/kg) of HP on days 1, 7 and 14 of pregnancy. The male pups were maintained under controlled conditions and the rats were killed 90 days after birth. The liver tissue was immediately excised, weighed and used for biochemical assays. RESULTS: The activity levels of succinate dehydrogenase (SDH), glutamate dehydrogenase (GDH), glucose-6-phosphate dehydrogenase (G-6-PDH), malate dehydrogenase (MDH) and aminotransaminases were significantly increased in the livers of rats exposed to HP during embryonic development. The lactate dehydrogenase (LDH) activity level was significantly decreased in the liver of experimental rats. Furthermore, there was a significant elevation of activity levels of antioxidant enzymes (glutathione S-transferase [GST] and catalase [CAT]) with an increased lipid peroxidation in the hepatic tissue of experimental rats compared with the control group. CONCLUSION: The results of the present study suggest that there is an increase in the oxidative metabolism, antioxidative mechanism and levels of lipid peroxidation in rats exposed to HP during embryonic development. The increased aminotransaminase activities in these rats reveal tissue damage and disruption of mitochondrial integrity.
Subject(s)
17-alpha-Hydroxyprogesterone/pharmacology , Embryo, Mammalian/drug effects , Liver/drug effects , 17-alpha-Hydroxyprogesterone/administration & dosage , Animals , Catalase/metabolism , Embryonic Development , Female , Glucosephosphate Dehydrogenase/metabolism , Glutamate Dehydrogenase/metabolism , Glutathione Transferase/metabolism , L-Lactate Dehydrogenase/metabolism , Lipid Peroxidation , Liver/embryology , Liver/enzymology , Liver/metabolism , Malate Dehydrogenase/metabolism , Male , Pregnancy , Rats , Rats, Wistar , Succinate Dehydrogenase/metabolism , Transaminases/metabolismABSTRACT
The present study was designed to assess potential reproductive toxicity caused by fentin and fenbutatin in the mice. Adult male mice received i.p. injections of fentin hydroxide and fenbutatin oxide at a dose of 0, 10 or 25 microg/kg body weight on 1st, 3rd and 5th day of experimentation. Mice were sacrificed on day 25 and analyzed for spermatogenesis and steroidogenesis. A significant decrease in epididymal sperm count, sperm motility, sperm viability and sperm function (HOS coiling) were observed in experimental mice when compared with controls. The decrease in sperm quantity and quality was significant in the 25 microg/kg group than that in the control group. The activity levels of testicular steroidogenic enzymes, 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and 17beta-hydroxysteroid dehydrogenase (17beta-HSD) were significantly decreased in treated mice indicating decreased steroidogenesis after organotin compounds administration. The levels of serum testosterone decreased with an increase in follicle stimulating hormone and luteinizing hormone in experimental mice when compared to control mice. The results suggest that fentin and fenbutatin cause impairment of spermatogenesis through the inhibition of testosterone production.
Subject(s)
17-Hydroxysteroid Dehydrogenases/metabolism , 3-Hydroxysteroid Dehydrogenases/metabolism , Organotin Compounds/toxicity , Spermatogenesis/drug effects , Testosterone/metabolism , Animals , Cell Survival/drug effects , Injections, Intraperitoneal , Male , Mice , Sperm Count , Sperm Motility/drug effects , Testis/drug effects , Testis/enzymology , Testis/metabolism , Testosterone/bloodABSTRACT
Hydroxyprogesterone caproate was administered to pregnant rats at a dose level of 10 and 25 mg/kg body weight on 1st, 7th and 14th gestational day and the male pups (F1 generation) were allowed to grow for 90 days. The effect of gestational exposure to hydroxyprogesterone caproate on fertility was assessed by breeding F1 male rats with control female rats besides analyzing sperm quality and quantity in F1 male rats. The number of implantation sites and viable fetuses was significantly reduced in females mated with F1 males that were exposed to hydroxyprogesterone caproate during embryonic development. The decrease in sperm function was associated with a decrease in sperm motility, sperm viability and sperm count in F1 rats. The study clearly indicates that in utero exposure to hydroxyprogesterone caproate affects fertility in male rats.
Subject(s)
Hydroxyprogesterones/pharmacology , Prenatal Exposure Delayed Effects , Reproduction/physiology , 17 alpha-Hydroxyprogesterone Caproate , Animals , Copulation , Embryo Implantation , Female , Fetal Resorption , Male , Pregnancy , Rats , Rats, Wistar , Reproduction/drug effects , Sex RatioABSTRACT
Sodium fluoride (NaF) administered orally to adult male rats at a dose level of 4.5 ppm and 9.0 ppm for 75 days caused significant decrease in the body weight, brain index and testicular index. A significant decrease in sperm count, sperm motility, sperm viability and sperm function (HOS positive) with increased sperm abnormalities was also observed in NaF-exposed male rats. The activity levels of testicular steroidogenic marker enzymes 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and 17beta-hydroxysteroid dehydrogenase (17beta-HSD) were significantly decreased in NaF-treated rats indicating decreased steroidogenesis and in turn spermatogenesis in rats exposed to NaF.
Subject(s)
Drinking , Fluorides/administration & dosage , Fluorides/pharmacology , Spermatogenesis/drug effects , Steroids/biosynthesis , Water/administration & dosage , Water/chemistry , 17-Hydroxysteroid Dehydrogenases/metabolism , Animals , Biomarkers/analysis , Body Weight/drug effects , Male , Rats , Rats, Wistar , Sperm Motility/drug effects , Spermatozoa/cytology , Spermatozoa/drug effects , Spermatozoa/physiologyABSTRACT
Hydroxyprogesterone caproate is one of the most effective and widely used drugs for the treatment of uterine bleeding and threatened miscarriage in women. Hydroxyprogesterone caproate was administered to pregnant rats in order to assess the effect of intraperitoneal exposure to supranormal levels of hydroxyprogesterone caproate on the male reproductive potential in the first generation. The cauda epididymal sperm count and motility decreased significantly in rats exposed to hydroxyprogesterone caproate during embryonic development, when compared with control rats. The levels of serum testosterone decreased with an increase in follicle stimulating hormone and luteinizing hormone in adult rats exposed to hydroxyprogesterone caproate during the embryonic stage. It was suggested that the impairment of male reproductive performance could be mediated through the inhibition of testosterone production.
Subject(s)
Hydroxyprogesterones/toxicity , Infertility, Male/chemically induced , Prenatal Exposure Delayed Effects , 17 alpha-Hydroxyprogesterone Caproate , Animals , Embryonic and Fetal Development/drug effects , Epididymis/abnormalities , Epididymis/embryology , Epididymis/pathology , Female , Hydroxyprogesterones/administration & dosage , Male , Pregnancy , Rats , Sperm Count , Sperm Motility/drug effectsABSTRACT
Pregnant Wistar strain albino rats were administered hydroxyprogesterone and the steroidogenic potential of the testis was analysed in the next generation adult male rats. In utero exposure to supranormal levels (10 mg/kg body weight or 25 mg/kg body weight) of hydroxyprogesterone decreased the activity levels of marker steroidogenic enzymes (3beta-hydroxysteroid dehydrogenase and 17beta-hydroxysteroid dehydrogenase) of adult (mature) rat testis. Hydroxyprogesterone mediation in the suppression of rat testicular steroidogenesis is suggested, which can be correlated to the observed decrease in male reproductive potential in mammals exposed to female hormones during embryonic development.