Biomarkers of imidacloprid toxicity in Japanese quail, Coturnix coturnix japonica.

The in vivo effect of the oral sublethal doses of 3.014 mg kg-1 of IMI (1/25 LD50) for 1, 7, 14, and 28 days every other day on Japanese quail was investigated. The results revealed that certain biomarkers in the selected tissues of the quail such as acetylcholinesterase (AChE), butyrylcholinesterase (BuChE), aminotransaminases (alanine aminotransferase, ALT, and aspartate aminotransaminase, AST), phosphatases (acid phosphatase, ACP, and alkaline phosphatase, ALP), lactate dehydrogenase (LDH), adenosine-triphosphatase (ATPase), glutathione-S-transferase (GST), lipid peroxidation (LPO), and blood glucose showed significant inductions, while significant reductions in the levels of glutathione-reduced (GSH), deoxyribonucleic acid (DNA), and ribonucleic acid (RNA) were noticed. In this study, the molecular mechanisms of the toxic effects of imidacloprid on quails were elucidated regarding neurotoxicity, hepatotoxicity, oxidative stress, lipid peroxidation, antioxidant activity, and genotoxicity. Because IMI induced alterations in the levels of these biomarkers in Japanese quail; therefore, Japanese quail as a wild avian can be used as a suite bioindicator to detect imidacloprid toxicity.

Effect of N-acetylcysteine on attenuation of chlropyrifos and its methyl analogue toxicity in male rats.

The attenuating effect of 150 mg/kg of N-acetylcysteine (NAC) against the oral administration of 7.88 and 202.07 mg/kg/day for 14 days of either chlropyrifos-ethyl (CPE-E) or chlropyrifos-methyl (CPF-M), respectively, in male rat was investigated using biochemical and genetic markers. Biomarkers such as acetylcholinesterase (AChE), butyrylcholinesterase (BuChE), paraoxonase (PON), adenosine 5'-triphosphatase (ATP-ase), glutathione-S-transferase (GST), catalase (CAT), glutathione reduced (GSH) in serum showed a significant decline in their levels, while calcium (Ca+2), cytochrome C reduction (CYC-R), lipid peroxidation (LPO), nitric oxide (NO) levels showed a significant increase in serum of treated rats. Regarding the genotoxic parameters, when rats are treated either with CPE-E or CPF-M, liver DNA, chromosomal aberration (CA), and micronucleated polychromatic erythrocytes (MnPCE) significantly increased, while the mitotic index (MI) and polychromatic erythrocytes (PCE)/ normochromatic erythrocytes (NCE) ratio were significantly decreased. However, the administration of NAC following the intoxication of CPF-E or CPF-M attenuated the tested biochemical and genotoxic markers. It can be concluded that NAC can be used to ameliorate the toxicity of certain organophosphorus compounds such as CPF-E and CPF-M.