Reduction in paraquat embryotoxicity by ascorbic acid in Xenopus laevis

The toxicity of herbicide Paraquat (PQ, 1-1'-dimethyl-4,4'bipyridylium dichloride) in animal cells is related to its rapid reduction and instantaneous reoxidation to produce the reactive oxygen species. Recently, the PQ evaluation with the Frog Embryo Teratogenesis Assay-Xenopus (FETAX) showed its high embryotoxicity. Supposing that the embryos' death was due to PQ-related oxidative damage, we used ascorbic acid (AA), a well known antioxidant, to reduce the PQ embryotoxicity in Xenopus laevis. Embryos were exposed from stage 8 to 47 to 0.1 mg/l PQ alone, and to PQ with AA concentrations ranging from 20 to 200 mg/l, using the FETAX procedure. PQ caused 72.2% mortality, while 17.1% of surviving larvae were affected by abnormal tail flexure. The PQ mortality percentages were reduced in a clear concentration-response by up to 15.2% in the group exposed to PQ with 200 mg/l AA. The histopathologic diagnoses revealed abnormal notochord flexure coupled with vesiculated, pear-shaped myocytes only in the PQ group. After embryo exposure to PQ with 200 mg/l AA, restoration of normal axial tail structures was evident. In conclusion, PQ embryotoxicity in X. laevis was most likely due to oxidative damage that was drastically reduced by AA.