ABSTRACT
Bisphenol A is a chemical used primarily as a monomer in the production of polycarbonate plastics and epoxy resins. It is a synthetic chemical compound that is produced in billions of pounds annually, and tagged as an endocrine disruptor. Bisphenol A is a high production synthetic chemical compound that is used in the production of many consumables and equipments of daily consumption and use by man. Growing interest in possible health threats posed by endocrine disrupting chemicals (bisphenol-A inclusive), as these substances are in our environment, food, and many consumer products. Therefore, this study aims to determine bisphenol-A effects on the hypothalamo-pituitary-ovarian axis, and role of melatonin in this regard. Forty-two Wistar rats were bred, grouped into 7, with each group consisting of 6 rats. Experimental groups were administered low and high doses of bisphenol-A and melatonin, starting from day 19, and was continued for 7 weeks orally. They were left to develop into full adults and were sacrificed on day 120±4 days. Blood samples, hypothalamus, pituitary and ovarian tissues were excised for biochemical and tissue antioxidants assays as well as genetic studies. Results show elevated gonadotropin and androgen levels. There was disruption of reactive oxygen species in the ovarian tissues, as well as alterations in the expression of genes that regulate reproduction at the hypothalamus and pituitary levels. Conclusion of early exposure to bisphenol-A is associated with prolonged duration of disruption of reproductive functions in female Wistar rats, which persist long after cessation of the exposure. Melatonin antioxidant effects give some promising outturns against bisphenol-A induced toxicities.
ABSTRACT
Bisphenol A is a chemical used primarily as a monomer in the production of polycarbonate plastics and epoxy resins. It is a synthetic chemical compound that is produced in billions of pounds annually, and tagged as an endocrine disruptor. Bisphenol A is a high production synthetic chemical compound that is used in the production of many consumables and equipments of daily consumption and use by man. Growing interest in possible health threats posed by endocrine disrupting chemicals (bisphenol-A inclusive), as these substances are in our environment, food, and many consumer products. Therefore, this study aims to determine bisphenol-A effects on the hypothalamo-pituitary-ovarian axis, and role of melatonin in this regard. Forty-two Wistar rats were bred, grouped into 7, with each group consisting of 6 rats. Experimental groups were administered low and high doses of bisphenol-A and melatonin, starting from day 19, and was continued for 7 weeks orally. They were left to develop into full adults and were sacrificed on day 120±4 days. Blood samples, hypothalamus, pituitary and ovarian tissues were excised for biochemical and tissue antioxidants assays as well as genetic studies. Results show elevated gonadotropin and androgen levels. There was disruption of reactive oxygen species in the ovarian tissues, as well as alterations in the expression of genes that regulate reproduction at the hypothalamus and pituitary levels. Conclusion of early exposure to bisphenol-A is associated with prolonged duration of disruption of reproductive functions in female Wistar rats, which persist long after cessation of the exposure. Melatonin antioxidant effects give some promising outturns against bisphenol-A induced toxicities.
ABSTRACT
Background: This study explored the efficacy of kolaviron—a biflavonoid complex isolatedfrom the seeds of Garcinia kola—in protecting against cuprizone (CPZ)-induced demyelination inboth the prefrontal cortex and the hippocampus of Wistar rats.Methodology: Thirty rats were treated to receive 0.5 mL phosphate-buffered saline (groupA, control), 0.5 mL corn oil (group B), 0.2% CPZ (group C), for 6 weeks, 0.2% CPZ for 3 weeks andthen 200 mg/kg of Kv for 3 weeks (group D), or 200 mg/kg of Kv for 3 weeks followed by 0.2%CPZ for 3 weeks (group E). Rats were assessed for exploratory functions and anxiety-like behaviourbefore being euthanised and perfused transcardially with 4% paraformaldehyde. Prefrontal andhippocampal thin sections were stained in hematoxylin and eosin and cresyl fast violet stains.Results: CPZ-induced demyelination resulted in behavioural impairment as seen byreduced exploratory activities, rearing behaviour, stretch attend posture, center square entry,and anxiogenic characteristics. Degenerative changes including pyknosis, karyorrhexis, neuronalhypertrophy, and reduced Nissl integrity were also seen. Animals treated with Kv showedsignificant improvement in behavioural outcomes and a comparatively normal cytoarchitecturalprofile.Conclusion: Kv provides protective roles against CPZ-induced neurotoxicity throughprevention of ribosomal protein degradation.