The Neutralizing Effect of Panax Ginseng for Toxicities in the Survival, Sperm Quality, Pregnancy and F1 Generation of Guinea Pigs Exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin / 대한비뇨기과학회지

PURPOSE: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), one of the most potent environmental pollutants, is known to disrupt the endocrine, immune, and reproductive system. This study was carried out to investigate the effect of a panax ginseng water extract (PG-WE) on the survival rate, sperm quality, and fertility impaired by TCDD. MATERIALS AND METHODS: Eighty male guinea pigs were divided into 8 groups. The normal control group received the vehicle and saline. TCDD was intraperitoneally injected at a single dose of 1microgram/kg. A PG-WE was administered at 100 or 200mg/kg/ day 1wk prior to (P groups) or subsequent to (C groups) TCDD-exposure for 12 and 10 weeks, respectively. The G groups received the vehicle and the PG-WE of 100 or 200mg/kg/day, respectively. The parameters for the male guinea pigs were assessed for 40 weeks. The effects on the F1 generation were assessed at a growth period of F1. RESULTS: All single TCDD-treated group animals died within 18 days and the survival rate of the PG-WE-treated groups increased in a dose dependant manner. Forty to 70% of the P and C groups survived until the 40th week and reached sexual maturation. The death rate of the progeny born from the PG-WE-treated groups was significantly lower than that in the NC group (14.3%). The M/F ratio of the F1 generation in the P and C groups had higher female birth ratio. The sperm number and morphology showed no significant differences among the groups. The PG-WE increased the sperm motility in the guinea pigs exposed to TCDD. CONCLUSIONS: Panax ginseng is a useful agent that can neutralize endocrine disrupters and environmental pollutants, and help maintain a high sperm quality after a growth period.

Effect of Panax Ginseng Water Extract for Treatment of Male Infertility / 대한남성과학회지

PURPOSE: We previously reported that Panax ginseng water extract (PG-WE) played both preventive and therapeutic roles on testicular toxicity induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in animal study, one of the most potent environmental pollutants. Thus we investigated whether PG-WE might be useful in the treatment of male infertility, because men in modern society are exposed by numerous environmental hormones. MATERIALS AND METHODS: Eighteen patients with abnormal semen analysis and 8 volunteers whose semen analysis were normal as control group were enrolled in this study. Before PG-WE administration, semen analysis, hormonal study, liver and renal function test, CBC, and urinalysis were checked in all subjects. PG-WE (2.4 gm) was administered everyday for 8 weeks in both groups. Follow-up semen analysis and laboratory studies were checked at 13th week. RESULTS: In patient group semen volume was increased (2.4 1.3 ml vs 2.6 1.6 ml, p=0.051). Semen volume as well as sperm concentration in oligospermia patient were increased but not significantly. Serum estradiol level decreased by PG-WE treatment in patient group (p=0.005). All subjects showed no toxic effect. CONCLUSIONS: Our data suggest that Panax ginseng is a potential agent that can improve abnormal sperm parameters in infertile male patients and also improve the sperm quality in healthy men.

Effects of Smoking and Polymorphisms of Glutathione S-Transferase M1 and T1 as Risk Factors on the Development of Bladder Cancer / 대한비뇨기과학회지

PURPOSE: To determine if the smoking status and polymorphisms of the glutathione S-transferase M1 (GSTM1) and T1 (GSTT1) genes were risk factors for bladder tumor and to evaluate the effects of their interaction on bladder tumor development. MATERIALS AND METHODS: One hundred and six patients with bladder cancer and 212 age- and sex-matched controls were enrolled in this study. Their smoking status was obtained from a self-completed questionnaire. The GSTM1 and GSTT1 polymorphisms were analyzed using a multiplex polymerase chain reaction (PCR) from the isolated genomic DNA. RESULTS: Smoking status was a strong risk factor for the development of bladder tumor (OR: 3.05, 95% CI: 1.46-6.34, p=0.001). The bladder tumor risk increased in the GSTM1-null genotype compared with the GSTM1-positive genotype (OR: 1.67, 95% CI: 1.02-2.72, p=0.041). On the other hand, the GSTT1-null genotype had significant protective effect against bladder tumor development (OR: 0.57, 95% CI: 0.35-0.91, p= 0.019). The GSTM1-null/GSTT1-positive genotypes had a significant risk factor for bladder tumors compared to the GSTM1-positive/GSTT1-null genotypes (OR: 3.05, 95% CI: 1.46-6.34, p=0.002). Smokers with the GSTM1-null/GSTT1-positive genotypes had a five-fold higher risk for developing bladder tumors than non-smokers with the same genotype and a nine-fold higher risk than non-smokers with the GSTM1-positive/ GSTT1-null genotypes (p=0.001). The GSTM1-null genotype in smokers also correlated with superficial bladder cancer (OR: 2.74, 95% CI: 1.01-7.41, p=0.04). CONCLUSIONS: Smoking is an independent risk factor for the development of bladder tumors in Korean, and the GSTM1-null and GSTT1-positive genotypes in smokers are important host risk factors. Therefore, smoking cessation particularly in individuals with the GSTM1-null/GSTT1-positive genotypes may prevent bladder tumor development.

Altered Expression of p33(ING1) in Human Bladder Cancer / 대한비뇨기과학회지

PURPOSE: p33(ING1) seems to be a candidate of novel growth inhibitor as a tumor suppressor gene and plays a critical role in regulation of cell cycle progression and susceptibility to apoptosis. In this study, we investigated p33(ING1) expression pattern in human bladder cancer and normal tissue. MATERIALS AND METHODS: RNA was extracted from 42 bladder cancer specimens and 24 normal bladder mucosa. Expression of p33(ING1) was examined by quantitative RT- PCR in which the ratio to GAPDH, an internal control, was used as a standardized expression value of the p33(ING1). Alterations of p33(ING1) expression between cancer and normal mucosa were compared and interrelationship with stage and grade was analyzed. To detect the mutations in the p33(ING1), PCR-SSCP analysis was also performed. RESULTS: Out of 42 bladder cancer (25 superficial and 17 invasive), 9 were grade I, 23 were grade II, and 10 were grade III. p33(ING1) expression in bladder cancer significantly decreased compared to that in normal bladder mucosa. The ratio of p33(ING1)/ GAPDH was 0.45 +/- 0.13 in bladder cancer, whereas for normal bladder mucosa this ratio was 0.66 +/- 0.17 (p <0.001). However, expression of p33(ING1) was neither correlated with tumor stage nor grade (p=0.489 and p=0.375, respectively). Changes in electrophoretic mobility of PCR-SSCP products were not detected in any of bladder cancers. CONCLUSIONS: These data suggest that decreased expression of p33(ING1) may contribute to the development of bladder cancer in part, even though the gene is mostly preserved. However, considering a discrepancy between the rate of mutation and the decreased expression, further study is warranted to determine the mechanism.