Evaluation of the effects of three arsenolipids on liver damage based on element imbalance and oxidative damage

Abstract

The International Agency for Research on Cancer has classified semimetal arsenic as a human carcinogen. Arsenic poisoning can severely impact human health. Arsenic can be classified into inorganic and organic arsenic, with arsenolipids (AsLs) belonging to the category of organic arsenic. The primary species of AsLs include arsenic‐containing hydrocarbons (AsHCs), fatty acids, and phospholipids. AsLs are highly abundant in marine organisms and diet may be the primary source of exposure to AsLs. Although increasing evidence shows that AsLs are cytotoxic to humans, the specific toxicity and its mechanism remain unclear. This study aimed to evaluate the hepatotoxicity and possible mechanisms of the toxic effects of AsLs in mice. Three AsLs (AsHC 332, AsHC 346, and AsHC 374) were administered via gavage at a dose of 3 mg/kg for 4 weeks. The results showed that short‐term exposure did not affect the normal growth and development of mice. However, it caused liver damage in mice, mainly by disrupting the metabolism of selenium, copper, zinc, and other elements related to the synthesis of antioxidant enzymes, thereby reducing the activity of antioxidant enzymes and the expression of related genes. The liver damage effect of AsHC 332 was the strongest among the three AsLs.