ABSTRACT
Consumption of fructose-rich food and exposure to endocrine disrupting chemicals continue to increase. High fructose consumption is associated with increased incidence of dyslipidemia, hypertension, hyperuricemia and insulin resistance. Bisphenol A (BPA) is an environmental contaminant that exhibits estrogen-like activity; it impairs reproductive organs, sperm production, spermatogenesis and fertility. We investigated the possible ameliorative effects of melatonin on rat epididymis and sperm characteristics following exposure to fructose and BPA. We used 42 adult male Sprague-Dawley rats divided into seven groups. Group 1, control group, was treated with 25 mg/kg sesame oil + 25 mg/kg 0.1% ethanol. Group 2 was treated with 10% aqueous fructose. Group 3 was treated with 25 mg/kg BPA. Group 4 was treated with 10% fructose and 25 mg/kg BPA. Group 5 was treated with 10% fructose and 20 mg/kg melatonin. Group 6 was treated with 25 mg/kg BPA and 20 mg/kg melatonin. Group 7 was treated with 10% fructose, 25 mg/kg BPA and 20 mg/kg melatonin. After 60 days, epididymal tissue was removed and analyzed using histochemistry and immunohistochemistry. Sperm were counted, and sperm motility and viability were investigated. Administration of BPA caused significant damage to both epididymal tissue and sperm quality; melatonin reduced the damage, but did not prevent it completely.
Subject(s)
Benzhydryl Compounds/pharmacology , Epididymis/drug effects , Fructose/pharmacology , Melatonin/pharmacology , Phenols/pharmacology , Spermatozoa/drug effects , Animals , Antioxidants/administration & dosage , Antioxidants/pharmacology , Benzhydryl Compounds/administration & dosage , Cell Survival/drug effects , Claudin-1/genetics , Claudin-1/metabolism , Epididymis/metabolism , Estrogens, Non-Steroidal/administration & dosage , Estrogens, Non-Steroidal/pharmacology , Fructose/administration & dosage , Gene Expression Regulation/drug effects , Male , Melatonin/administration & dosage , Occludin/genetics , Occludin/metabolism , Phenols/administration & dosage , Rats , Rats, Sprague-Dawley , Sweetening Agents/administration & dosage , Sweetening Agents/pharmacology , Zonula Occludens-1 Protein/genetics , Zonula Occludens-1 Protein/metabolismABSTRACT
Diabetes mellitus (DM) affects many organs including kidney. Tyrosine kinase can cause hypoglycemia and sunitinib is an inhibitor of tyrosine kinase. We investigated the possible effects of sunitinib on the kidney of streptozotocin (STZ) induced type 1 diabetic mice. We used 28 CD 1 type male mice divided into four groups of seven. Type 1 diabetes was induced by injection of STZ. Group 1 was the untreated control. Group 2 comprised non-diabetic mice + sunitinib. Both groups 1 and 2 exhibited normal blood glucose levels. Group 3 comprised STZ treated diabetic mice + saline. Group 4 were diabetic mice + sunitinib treatment. Kidneys were removed after 8 weeks. The immunoreactivities of vimentin, E-cadherin and S100 were assessed. Immunostaining of vimentin, E-cadherin and S100 was located in both the glomeruli and tubules of the kidney. We found that the number of vimentin and E-cadherin positive glomeruli and tubules were increased after sunitinib treatment compared to saline treated diabetic mice. The number of vimentin labeled tubules was decreased in the sunitinib treated group compared to diabetic + saline groups. Differences in the number of S100 positive tubules and glomeruli between groups 3 and 4 were not statistically significant. The effect of sunitinib on experimental diabetic mice appears to be related to levels of vimentin, E-cadherin and S100 in the glomeruli and tubules of the kidney, and sunitinib may protect against renal damage from DM.
