Toxicity

The toxicity of OA varies considerably with dose and between species. Dogs and pigs are the most sensitive species (0.2 and 1 mg/kg body weight, respectively). Synergistic effects of OA with other mycotoxins, such as citrinin and penicillic acid, on the LD50 were seen in mice following intraperitoneal injection. OA is nephrotoxic to a number of animal species, and the presence of OA in feed is believed to be the most important cause of spontaneous myco-toxic porcine and poultry nephropathy. OA also produces hepatic toxicity at high doses. OA is ter-atogenic in mice, rats, and hamster, and the major target in the fetus is the developing central nervous system. OA is also immunosuppressive at low doses, affecting immune function at both the level of antibody synthesis and natural killer cell activity. The toxic mechanism of OA has been shown to be inhibition of protein synthesis by competition with phenylalanine in the phenylalanyl-tRNA synthetase-catalyzed reaction. OA also inhibits other enzymes that use phenylalanine as a substrate, such as phe-nylalanine hydroxylase. The effect of OA on protein synthesis is followed by an inhibition of RNA synthesis, which may affect proteins with a high turnover. OA has also been found to enhance lipid peroxidation in vivo.

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