Abstract
Patulin (PAT) is a toxic fungal metabolite, and oxidative damage was proved to be its important toxicity mechanism. Selenium nanoparticles (SeNPs) were prepared by reducing sodium selenite with chitosan as a stabilizer and used for preventing PAT-induced liver, kidney and gastrointestinal damage. SeNPs have good dispersibility, in vitro antioxidant activity, and are much less cytotoxic than sodium selenite. Cell culture studies indicated that SeNPs can effectively alleviate PAT-induced excessive production of intracellular ROS, the decline of glutathione peroxidase activity, and the suppression of cell viability. Evaluation of serum biochemical parameters, histopathology, oxidative stress biomarkers and activities of antioxidant enzymes in a mouse model showed that pre-treatment with SeNPs (2 mg Se/kg body weight) could ameliorate PAT-induced oxidative damage to the liver and kidneys of mice, but PAT-induced gastrointestinal oxidative damage and barrier dysfunction were not recovered by SeNPs, possibly because the toxin doses suffered by the gastrointestinal as the first exposed tissues exceeded the regulatory capacity of SeNPs. These results suggested that a combination of other strategies may be required to completely block PAT toxicity.
Highlights
Patulin (PAT) is an unsaturated heterocyclic lactone produced by several fungal species of Penicillium, Aspergillus and Byssochlamys
Pre-treatment with SeNPs reduced liver and kidney oxidative damage caused by PAT administration, but did not diminish or reverse PAT-induced gastrointestinal lesions
The SeNPs used in this work was prepared by ascorbic acid reduction with sodium selenite as the selenium source and CTS as the stabilizer
Summary
Patulin (PAT) is an unsaturated heterocyclic lactone produced by several fungal species of Penicillium, Aspergillus and Byssochlamys. This water-soluble and thermostable mycotoxin is present in many vegetables and fruits (especially apples), as well as in cereals, tea, and silage [1]. PAT was originally discovered as a wide-spectrum antibiotic, it was reclassified as a hazard for its potential negative health effects. Chronic, and cellular toxicities of PAT have been reported by a wide number of studies [2]. The acute symptoms of PAT consumption include agitation, convulsions, vomiting, and organ damage such as kidney, liver, lung and gastrointestinal [3]. The toxic effects of PAT at cellular level include causing DNA damage and protein inactivation, inhibiting the synthesis of some key enzymes, and inducing apoptosis, etc. The toxic effects of PAT at cellular level include causing DNA damage and protein inactivation, inhibiting the synthesis of some key enzymes, and inducing apoptosis, etc. [4]
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