Current study was designed to evaluate the effects of β-cyfluthrin, as a toxicant substance, and trans -ferulic acid ( trans - FA ), as a protective agent, on different parameters of rooster semen upon liquid storage. For this purpose, semen samples of roosters (Ross 308, n = 10, 32-wk-old) were collected twice a week. Good quality samples (≥70% progressive motion) were diluted, pooled and then divided for the purposes of the study. In the first experiment, motility of spermatozoa was evaluated following exposure to different concentrations of β-cyfluthrin (1, 2.5, 5, 10, 20, 40, and 80 µM) at 0, 24, and 48 h of storage. In the second experiment, constant doses of β-cyfluthrin (10 µM) alone or in combination with trans -FA (10, 25 mM) were assessed on motility and viability of spermatozoa at 0, 24, and 48 h time points. Moreover, amounts of malondialdehyde ( MDA ), total antioxidant capacity ( TAC ), total nitrate-nitrite, total hydroperoxide ( HPO ), and activity of superoxide dismutase ( SOD ) were evaluated in the homogenate of spermatozoa-diluent at studied time points. Results of the first experiment showed that amounts of β-cyfluthrin greater than 5 µM, significantly reduced the motility of spermatozoa at 24 and 48 h of storage ( P < 0.05). The second experiment demonstrated that, trans -FA especially at 10, 25 mM doses restored the motility and viability of spermatozoa compared to β-cyfluthrin treated group ( P < 0.05). Amounts of MDA (10, 25 mM), hydroperoxide (10, 25, and 50 mM), and nitrate-nitrite (10, 25, and 50 mM) were lower and TAC (10 and 25 mM) were greater in trans -FA + β-cyfluthrin treated groups compared to β-cyfluthrin alone treated samples ( P < 0.05). However, activity of SOD did not show significant changes by the treatment ( P > 0.05). It seems that trans -FA could ameliorate toxic effect of β-cyfluthrin via reduction of peroxidative (as evident by measurement of MDA) and nitrosative (as evident by measurement of nitrate-nitrite) reactions over cold preservation of rooster semen.

Clothianidin (CTD) is a member of the neonicotinoid group of insecticides. This study was performed to determine the effect of quercetin on clothianidin-induced liver injury (CTD) in rats. Rats were randomly assigned to a normal control (saline), a CTD control-treated group (20 mg/kg) every 3 days for 21 days, and CTD + quercetin-treated groups (2.5, 5, and 10 mg/kg) for 35 days intraperitoneally. Enzyme activity, including alanine aminotransferase (ALT) and aspartate aminotransferase (AST), was measured by spectrophotometry in serum samples by an automatic biochemical analyzer using commercial kits. Total antioxidant capacity (TAC), malondialdehyde (MDA), and nitrate-nitrite were measured in homogeneous liver tissue samples of animals. A significant increase in ALT and AST enzyme activity was observed in the CTD group in comparison with that of the control groups. In the clothianidin + quercetin (10 mg/kg) group, the ALT and AST enzyme levels decreased compared to the clothianidin control group significantly P < 0.05 . The MDA value of the liver increased in the clothianidin-treated group compared to that of the control groups P < 0.05 . Decreased tissue TAC level was observed in the CTD-treated group in comparison with that of the control groups P < 0.05 . The MDA level of the liver decreased in the clothianidin + quercetin (10 mg/kg) group compared to that of the CTD control group P < 0.05 . Quercetin significantly raised the level of TAC in the liver tissue of the clothianidin + quercetin (10 mg/kg) treated group compared to that of the clothianidin control group P < 0.05 . Liver nitrate-nitrite measurement showed a significant increase in the clothianidin group compared to that of the normal control group P < 0.05 . Nitrate-nitrite level in the liver was decreased in clothianidin + quercetin (10 mg/kg) compared to that of the clothianidin control group significantly P < 0.05 . Histopathological investigation revealed that contact to the CTD induced tissue disorganization and inflammatory cell infiltration, but minor histopathological alterations in the liver tissues of rats treated with CTD and quercetin (10 mg/kg) were detected.

The current study was designed to evaluate the possible protective effects of luteolin against β-cyfluthrin-mediated toxicity on the primary culture of rat hepatocytes (RHs). In the first step, the exposure of RHs to β-cyfluthrin (10, 20, 40, and 80 μM) was assessed by MTT. Second, redox condition was evaluated in cotreatment of cells with luteolin (20, 40, and 60 μM) and β-cyfluthrin (40 μM) at both medium and intra levels. In comparison to control, viability was lower in 40 and 80 μM β-cyfluthrin-treated groups at 24 h and all β-cyfluthrin-treated groups at 48 h ( P < 0.05 ). Cotreatment with 20 or 40 μM luteolin + 40 μM β-cyfluthrin resulted in a higher viability value compared to β-cyfluthrin alone at 24 and 48 h of incubation ( P < 0.05 ). Administration of 20 or 40 μM luteolin with β-cyfluthrin led to the decrease of malondialdehyde and total nitrate/nitrite and the increase of total antioxidant capacity (TAC) values in both medium and intrahepatocyte levels compared to the β-cyfluthrin-treated group at 48 h ( P < 0.05 ). It seems that low and medium doses of luteolin possess the potential to reduce β-cyfluthrin-mediated hepatotoxicity via attenuation of peroxidative/nitrosative reactions and augmentation of TAC levels.

The current study was conducted to evaluate the different concentrations of deltamethrin (DEL; Exp. 1) and the protective role of idebenone (IDB) supplemented with toxic dose of deltamethrin (Exp. 2) during chilled storage of ram semen. Collected samples were pooled and diluted at 500×106 spermatozoa per mL. In Exp. 1, effect of DEL at 1, 2.5, 5, 10, 20, 40, 80 μM levels were evaluated on different variables of spermatozoa motion characteristics. In Exp. 2, different amounts of IDB (2, 4, and 8 μM) concurrent with constant doses of DEL (10 μM) were examined on semen quality upon chilled preservation up to 72 h. Indices of spermatozoa kinematics, functionality of plasma membrane and viability were recorded. Biochemical metabolites were measured in spermatozoa and its medium (extender) at different time points. In Exp.1, different parameters of spermatozoa kinematics were affected by exposure to DEL in a dose dependent manner. In Exp. 2, combination of IDB with DEL, resulted in a significant (P < 0.05) increase in total motility, forward progressive motility and curvilinear path velocity compared to DEL group at 24, 48 and 72 h. Simultaneous administration of IDB with DEL increased the percentage of spermatozoa with functional membrane and viability compared to DEL group at 72 h (P < 0.05). The amounts of lipid peroxidation index were lower in medium of combination groups compared to DEL group at 48 h and 72 h (P < 0.05). Antioxidant capacity were higher in spermatozoa and medium of IDB treated groups compared to DEL group at 72 h (P < 0.05). Amounts of total nitratenitrite and superoxide dismutase activity of spermatozoa and medium did not affect by treatment (P > 0.05). In conclusion, IDB could ameliorate oxidative and peroxidative damages induced by DEL mild toxicity upon cold preservation of ram semen.

The current study was designed to investigate the in ovo injection of formic acid (FA) on hatchability rate (HR; Experiment 1) and the potential ameliorative role of kinetin concurrent with FA on biochemical parameters of hatched broilers (Experiment 2). In Experiment 1, live embryonated eggs (n = 280; Day 4 of incubation) were in ovo injected with 0.03, 0.06, 0.125, 0.25, 0.50, 1, 2, 4, 8, 16 and 32 m m FA. In Experiment 2, intra‐yolk‐sac administration of toxic doses of FA (2 m m) concurrent with kinetin at 50, 100 or 200 µ m were evaluated on hatched embryos. The amount of malondialdehyde (MDA), total antioxidant capacity (TAC), total nitrate–nitrite (TNN), total lipid hydroperoxide (TLHP) and superoxide dismutase (SOD) activity was measured in serum, liver, heart and brain tissues. The results revealed that injection of 2 mM FA significantly increased mortality compared to the control group (p < 0.05). Concurrent administration of 50 or 100 µ m kinetin + 2 m m FA increased HR to 10% and 20% compared to the FA‐alone‐treated group, respectively. Intra‐yolk‐sac‐received FA group showed greater amounts of MDA, TLHP and TNN and lesser amounts of TAC and SOD activity in serum and tissue samples of liver, heart and brain compared to control groups (p < 0.001). In comparison to the FA‐alone‐treated group, all doses of kinetin were able to increase the TAC levels in serum and tissue samples when administered concurrently with FA. The doses of 50 and 100 µ m kinetin were efficacious to ameliorate the toxic role of FA injection on SOD activities (p < 0.001). Co‐injection of 100 µ m kinetin plus FA significantly reduced the amounts of MDA, TNN and TLHP in measured samples compared to the FA‐alone‐injected group (p < 0.001). Our results indicated that kinetin (especially at 100 µ m doses) would ameliorate the toxic effects of FA on developing live chicken embryos.