• Korean Journal of Oriental Medicine
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• v.12 no.1
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• pp.91-102
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• 2006

We treated KunYangDan (KYK) in SD rats in order toexamine the protective effect against cell damage induced by diethylhexyl phthalate (DEHP). KYD reduced DEHP toxicity by increasing the function of immune cell numbers weight increase of spleen.red blood cells,HB,and HCT content,sperm number and mobility,resulting in improving reproductive function by judging from the recovery of testosterone content. Interestingly the hormone change of testosterone by KYD significantly recovered the decreased its leve. Taken together,these results suggest that KYD specifically affect the reproductive function induced by DEHP,an endocrine disruptor.

• Clinical and Experimental Reproductive Medicine
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• v.43 no.4
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• pp.193-198
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• 2016

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 $H_2O_2$. We hypothesized that G6PD deficiency may reduce the amount of NADPH in sperms, thereby inhibiting the detoxification of $H_2O_2$, 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 $120{\mu}M$ concentrations of $H_2O_2$. After 1 hour incubation at $37^{\circ}C$, sperms were evaluated for motility and viability. Results: Incubation of sperms with 10 and $20{\mu}M\;H_2O_2$ led to very little decrease in motility and viability, but motility decreased notably in both groups in 40, 60, and $80{\mu}M\;H_2O_2$, and viability decreased in both groups in 40, 60, 80, and $120{\mu}M\;H_2O_2$. 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 $H_2O_2$, and the reducing equivalents necessary for protection against $H_2O_2$ are most likely produced by other pathways. Therefore, G6PD deficiency cannot be considered as major risk factor for male infertility.

• Journal of Radiation Protection and Research
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• v.32 no.4
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• pp.184-189
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• 2007

In order to investigate the enhancement effects of low dose radiation on biological activation, this study applied low dose X-ray to the whole body of male rats to find out whether hormesis is induced in male germ cells. Total 36 Sprague-Dawley(SD) rats as experimental animal were subdivided into 6 groups(in 6 rats per group) such as control, 10 mGy, 20 mGy, 50 mGy, 100 mGy and 200 mGy radiation group All the groups showed slightly increasing number of sperms per 0.1g semen ($14.216{\times}10^6,\;13.901{\times}10^6,\;14.153{\times}10^6,\;13.831{\times}10^6,\;14.137{\times}10^6,\;14.677{\times}10^6$ respectively), and the motility of sperms amounted to 50.9%, 49.5%, 55.1%, 54.3%, 48.0% and 52.2% respectively. Particularly, compared to the control, the other 5 groups showed higher male hormone level, and the microscopic observations of testicle tissues showed no vacuolization in seminiferous tubules and testis cells. In the results of this experiment, no harmful effect was observed on Sprague-Dawley (SD) rats for which the dose of radiation was controlled as regulated legally by the Ministry of Science and Technology and the Ministry of Health and Welfare. However, as these results were obtained from a limited number of animals, we cannot maintain that the same effect will be observed in the human body. Therefore, there should be further research on the effect on other animals and ultimately on the human body.