Glucose-6-phosphate dehydrogenase deficiency does not increase the susceptibility of sperm to oxidative stress induced by H(2)O(2)

OBJECTIVE: Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common human enzyme defect. G6PD plays a key role in the pentose phosphate pathway, which is a major source of nicotinamide adenine dinucleotide phosphate (NADPH). NADPH provides the reducing equivalents for oxidation-reduction reductions involved in protecting against the toxicity of reactive oxygen species such as H(2)O(2). We hypothesized that G6PD deficiency may reduce the amount of NADPH in sperms, thereby inhibiting the detoxification of H(2)O(2), which could potentially affect their motility and viability, resulting in an increased susceptibility to infertility. METHODS: Semen samples were obtained from four males with G6PD deficiency and eight healthy males as a control. In both groups, motile sperms were isolated from the seminal fluid and incubated with 0, 10, 20, 40, 60, 80, and 120 µM concentrations of H(2)O(2). After 1 hour incubation at 37℃, sperms were evaluated for motility and viability. RESULTS: Incubation of sperms with 10 and 20 µM H(2)O(2) led to very little decrease in motility and viability, but motility decreased notably in both groups in 40, 60, and 80 µM H(2)O(2), and viability decreased in both groups in 40, 60, 80, and 120 µM H(2)O(2). However, no statistically significant differences were found between the G6PD-deficient group and controls. CONCLUSION: G6PD deficiency does not increase the susceptibility of sperm to oxidative stress induced by H(2)O(2), and the reducing equivalents necessary for protection against H(2)O(2) are most likely produced by other pathways. Therefore, G6PD deficiency cannot be considered as major risk factor for male infertility.