In ovo exposure of a Fusarium mycotoxin butenolide induces hepatic and renal oxidative damage in chick embryos, and antioxidants provide protections

• Published in: Toxicology in vitro 2009-10, Vol.23 (7), p.1354-1359
• Main Authors: Wang, Yi-Mei, Wang, Hui-Jiao, Peng, Shuang-Qing
• Format: Article
• Language: English
• Subjects: 4-Butyrolactone - administration & dosage; 4-Butyrolactone - analogs & derivatives; 4-Butyrolactone - toxicity; Animals; Antioxidant; Antioxidants - pharmacology; Ascorbic Acid - pharmacology; Butenolide; Chick Embryo; Fusarium; Glutathione Peroxidase - metabolism; In ovo exposure; Injections; Kidney - metabolism; Lipid Peroxidation - drug effects; Liver - metabolism; Models, Animal; Mycotoxins - administration & dosage; Mycotoxins - toxicity; Ovum; Oxidative damage; Oxidative Stress - drug effects; Protective Agents - pharmacology; Sodium Selenite - pharmacology; Superoxide Dismutase - metabolism
• ISSN: 0887-2333; 1879-3177
• DOI: 10.1016/j.tiv.2009.06.028

Butenolide is a mycotoxin produced by several toxigenic Fusarium species. It frequently invades many important grains, and evokes a broad spectrum of toxic effects. For these reasons, butenolide poses a health risk to both humans and animals. However, many toxicology issues of butenolide including targets and mechanisms of toxicity remain to be elucidated so far. The present study therefore attempts to reveal the toxic profile of butenolide from a viewpoint of oxidative damage, using chick embryos as an in vitro model. A single in ovo injection of butenolide resulted in significant oxidative injuries in embryonic livers and kidneys, as manifested by a dose-dependent depletion of sulfhydryl groups, reduction of glutathione peroxidase activity, and increase of thiobarbituric acid reactive substances production, an indicator of lipid peroxidation. In contrast, co-injections of butenolide with antioxidants sodium selenite, vitamin C and a representative antioxidative enzyme superoxide dismutase markedly abated these oxidative toxicities. In conclusion, the present study suggests that oxidative damage may serve as a mediator in the toxicity of butenolide, and amelioration of antioxidant defense capacity by exogenous supplementation may play a role in the prevention and treatment of butenolide intoxication.