Vitamin C exerts novel protective effects against cadmium toxicity in mouse spermatozoa by inducing the dephosphorylation of dihydrolipoamide dehydrogenase.

Cadmium (Cd) has been reported to inhibit mouse sperm motility by inducing the tyrosine phosphorylation of dihydrolipoamide dehydrogenase (DLD). This study aimed to assess the potential effects of vitamin C (Vc) on ameliorating Cd-induced tyrosine phosphorylation of DLD and the specific underlying mechanism. Vc induced the dephosphorylation of DLD or inhibited the tyrosine phosphorylation of DLD. Accordingly, DLD activity, nicotinamide adenine dinucleotide hydrogen (NADH) levels, ATP levels and motility parameters were all restored to normal levels by Vc. Moreover, the effects of Vc on ameliorating these indicators had striking similarities to the effects of ethylenediaminetetraacetic acid (EDTA). In addition, neither the antioxidant melatonin nor the universal oxidant H