The toxicity of herbicide Paraquat (PQ, 1-1'-dimethyl-4,4'bipyridylium dich
loride) in animal cells is related to its rapid reduction and instantaneous
reoxidation to produce the reactive oxygen species. Recently, the PQ evalu
ation with the Frog Embryo Teratogenesis Assay-Xenopus (FETAX) showed its h
igh 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 rangin
g 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. T
he 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 histopathol
ogic diagnoses revealed abnormal notochord flexure coupled with vesiculated
, pear-shaped myocytes only in the PQ group. After embryo exposure to PQ wi
th 200 mg/l AA, restoration of normal axial tail structures was evident. In
conclusion, PQ embryotoxicity in X. laevis was most likely due to oxidativ
e damage that was drastically reduced by AA. (C) 2001 Elsevier Science B.V.
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