BACKGROUND: Paraquat poisoning is one of leading intoxication worldwide without an effective antidote and treatment protocol. Among the other organs, cardiotoxicity of paraquat has been frequently reported. AIM: The protective effects of atorvastatin (STN) on paraquat-induced cardiotoxicity and the role of peroxisome proliferator-activated receptors γ in the mediation of STN effects were investigated. METHODS: Forty-two male Wistar rats were aliquoted into control or test groups. The animals in test groups in addition of paraquat received saline normal (PQ), pioglitazone (PGT), atorvastatin (STN), PGT + STN, PGT + GW9662, and/or STN + GW9662 for 14 days. RESULTS: PGT and STN lowered lipid peroxidation rate, nitric oxide concentration, and activity of myeloperoxidase and CK/MB in the heart. PGT and STN protected from thiol molecules reduction and PQ-induced histopathological injuries. STN regulated the PQ-induced upregulation of COX-II expression in the heart. All STN-related protective effects were reversed by GW9662 as PPARγ antagonist. CONCLUSIONS: These data suggest a cardioprotective effect for STN against the PQ-induced inflammation and oxidative stress. The pharmacologic approach of these findings indicates that STN through PPARγ pathway lowered the PQ-induced cardiotoxicity.
Antioxidants/pharmacology , Atorvastatin/pharmacology , Heart Diseases/prevention & control , Myocytes, Cardiac/drug effects , Oxidative Stress/drug effects , PPAR gamma/agonists , Paraquat , Animals , Cardiotoxicity , Creatine Kinase, MB Form/metabolism , Cyclooxygenase 2/genetics , Cyclooxygenase 2/metabolism , Disease Models, Animal , Heart Diseases/chemically induced , Heart Diseases/metabolism , Heart Diseases/pathology , Lipid Peroxidation/drug effects , Male , Myocytes, Cardiac/metabolism , Myocytes, Cardiac/pathology , Nitric Oxide/metabolism , PPAR gamma/metabolism , Peroxidase/metabolism , Rats, Wistar , Signal Transduction , Sulfhydryl Compounds/metabolism
This study was performed to investigate in vitro effects of deoxynivalenol (DON) on mice sperm quality parameters including viability, motility and DNA damages at various concentrations and exposure times. Mice spermatozoa were exposed to DON at 0, 2.5, 5 and 10 µM for 1, 3 and 6 hr, motility parameters were evaluated by computer-assisted analysis and viability was examined by colorimetric metabolic activity assay and HOS test. DNA damage was examined by acridine orange staining, and sperm damages via lipid peroxidation pathway were determined by malondialdehyde (MDA) content measurement. DON affected sperm parameters in a concentration- and time-dependent manner. In all test groups, the average path velocity and progressive motile spermatozoa were remarkably reduced. In comparison with the controls, after 1, 3 and 6 hr exposure to DON, viability of spermatozoa was reduced 25, 30 and 49% respectively. DON exposure at 10 µM for 6 hr resulted in 15% DNA damage and 2.5-fold more MDA generation, when compared with nonexposed spermatozoa. Our data suggest that DON causes sperm quality parameters decline in concentration- and time-dependent fashion, which attribute to the reduction in sperm metabolic activity and membrane integrity and equally to increase in lipid peroxidation rate and DNA damage.
Chromatin/radiation effects , DNA Damage/radiation effects , Sperm Motility/drug effects , Spermatozoa/drug effects , Trichothecenes/toxicity , Animals , Fusarium/chemistry , Lipid Peroxidation/drug effects , Male , Malondialdehyde/metabolism , Mice , Mice, Inbred BALB C , Models, Animal , Oxidative Stress/radiation effects , Reactive Oxygen Species/metabolism , Semen Analysis , Spermatozoa/metabolism
