Antioxidant vitamin E protects embryos of Xenopus tropicalis against lambda-cyhalothrin induced embryotoxicity

Pesticides are capable of increasing risks to the early development of nontarget organisms through oxidative stress. The supplementation of antioxidants could help to modulate the toxic effects of pesticides, but much remains to be understood in the interactions between pesticides and antioxidants in amphibians. In the present study, the embryotoxicity of a widely used pyrethroid, lambda-cyhalothrin (LCT), and the potential effect of α-tocopherol (TOC) on embryos of Xenopus tropicalis were evaluated. Exposure to LCT did not affect the hatch rate, survival, or body length of the embryos. However, environmentally relevant concentrations of LCT could induce significant malformations on the larvae. Exposure to LCT led to a concentration-dependent induction of oxidative stress and cytotoxicity that subsequently resulted in embryotoxicity. During the early developmental stages, vitamin E could work as a powerful protective antioxidant. The LCT-induced overproduction of reactive oxygen species and increased enzymatic activities were fully inhibited by treatment with 1 μg/L TOC. However, only supplementation with 100 μg/L TOC provided partial protection against the morphological changes caused by LCT. The results from the present study suggest that antioxidant vitamin E possesses protective potential against pyrethroid-induced embryotoxicity in amphibian embryos through the prevention of oxidative stress.