Butachlor, one of the most widely used
herbicides in agriculture, has been reported with high ecotoxicity to aquatic plants and animals. In this study, a (1)H NMR based metabolomics approach combined with histopathological examination and biochemical assays was applied to comprehensively investigate the toxic effects of
butachlor on four important organs (gill, brain, liver and kidney) of goldfish (Carassius auratus) for the first time. After 10 days'
butachlor exposure at two dosages of 3.2 and 0.64 μmol/L, fish tissues (gill, brain, liver and kidney) and serum were collected. Histopathological inspection revealed severe impairment of gill filaments and obvious cellular
edema in livers and kidneys. The increase of
glutathione peroxidase (GSH-Px) activity in gill and methane dicarboxylic
aldehyde (MDA) level in four tissues reflected the disturbance of antioxidative system in the intoxicated goldfish. Serum
lactate dehydrogenase (LDH) activity and
creatinine (CRE) level were increased in
butachlor exposure groups, suggesting liver and kidney
injuries induced by
butachlor. Orthogonal signal correction partial least-squares discriminant analysis (OSC-PLS-DA) of NMR profiles disclosed metabolic changes that were related to the toxic effects of
butachlor including oxidative stress, disorder of energy metabolism and
amino acids metabolism, and disturbance of
neurotransmitter balance in
butachlor exposed goldfish. This integrated metabolomics approach provided a molecular basis underlying the toxicity of
butachlor and demonstrated that metabolomics was a powerful and highly effective approach to elucidate the toxicity and underlying mechanisms of
herbicides and pesticides, applicable for their risk assessment.