Panax ginseng protects the testis against 2,3,7,8-tetrachlorodibenzo-p-dioxin induced testicular damage in guinea pigs

2001 ◽  
Vol 83 (7) ◽  
pp. 842-849 ◽  
Author(s):  
Kim ◽  
Hwang ◽  
Lee ◽  
Song ◽  
Kim
1995 ◽  
Vol 69 (10) ◽  
pp. 677-683 ◽  
Author(s):  
Mikko Unkila ◽  
Marjatta Ruotsalainen ◽  
Raimo Pohjanvirta ◽  
Matti Viluksela ◽  
Ewen MacDonald ◽  
...  

1986 ◽  
Vol 84 (3) ◽  
pp. 439-453 ◽  
Author(s):  
Ching-Jang Huang Lu ◽  
Raymond B. Baggs ◽  
David Redmond ◽  
Ellen C. Henry ◽  
Arnold Schecter ◽  
...  

Reproduction ◽  
2017 ◽  
Vol 153 (6) ◽  
pp. 737-747 ◽  
Author(s):  
Min Kyoung Kim ◽  
Kyu-Min Cha ◽  
Seock-Yeon Hwang ◽  
Un-Kyu Park ◽  
Seok Kyo Seo ◽  
...  

Testicular hyperthermia is well studied to cause impaired spermatogenesis. In the present study, the protective effect of enzymatically modified (pectinase-treated)Panax ginseng(GINST) against intermittent sub-chronic heat stress-induced testicular damage in rats was investigated. Male Sprague–Dawley rats were divided into four groups: normal control (NC), heat-stressed control (HC), heat-stressed plus GINST-100 mg/kg/day (HG100) and heat-stressed plus GINST-200 mg/kg/day (HG200) treatment groups. GINST (100 and 200 mg/kg/day) was mixed separately with a regular pellet diet and was administered orally for 8 weeks starting from 1 week before heat exposure. Parameters such as organ weight, blood chemistry, sperm kinetic values, expression of antioxidant enzymes, spermatogenesis molecules and sex hormone receptors levels were measured. Data revealed that kidney and epididymis weight were significantly (P < 0.05) decreased with heat stress and recovered by GINST treatment. Further, the altered levels of blood chemistry panels and sperm kinetic values in heat stress-induced rats were attenuated when GINST was administered (P < 0.05). Furthermore, the expression levels of antioxidant-related enzymes (GSTM5 and GPX4), spermatogenesis-related proteins (CREB1 and INHA) and sex hormone receptors (androgen receptor, luteinizing hormone receptor and follicle-stimulating hormone receptor) were reduced by heat stress; however, GINST treatment effectively ameliorated these changes. In conclusion, GINST was effective in reducing heat-induced damage in various male fertility factorsin vivoand has considerable potential to be developed as a useful supplement in improving male fertility.


Andrologia ◽  
2012 ◽  
Vol 45 (4) ◽  
pp. 225-231 ◽  
Author(s):  
F. Oguz ◽  
O. Ciftci ◽  
M. Aydın ◽  
N. Timurkaan ◽  
A. Beytur ◽  
...  

1985 ◽  
Vol 5 (4) ◽  
pp. 700-712
Author(s):  
CHRISTOPHER K. KELLING ◽  
BRIAN J. CHRISTIAN ◽  
STANLEY L. INHORN ◽  
RICHARD E. PETERSON

2004 ◽  
Vol 94 (4) ◽  
pp. 663-668 ◽  
Author(s):  
Seock-Yeon Hwang ◽  
Wun-Jae Kim ◽  
Jae-Joon Wee ◽  
Jong-Soon Choi ◽  
Si-Kwan Kim

1953 ◽  
Vol 97 (5) ◽  
pp. 711-726 ◽  
Author(s):  
Jules Freund ◽  
Murray M. Lipton ◽  
George E. Thompson

The injection into the dorsal skin of a suspension of guinea pig testis or spermia incorporated in a water-in-oil emulsion containing killed mycobacteria induces aspermatogenesis in guinea pigs. The injury begins with the inhibition of the maturation of spermia and proceeds through the degeneration and exfoliation of spermatids, spermatocytes, and finally spermatogonia. These germinal cells pass from the seminiferous tubules into the epididymis. The process is not associated with inflammation. No significant changes occur in the intertubular spaces and the Leydig cells do not seem to be affected. The seminal vesicles and the prostate remain normal. The aspermatogenesis may begin in 10 days and it lasts for more than 5 months. The process may lead to atrophy of the seminiferous tubules and fibrosis. Guinea pigs which receive a suspension of their own testis or spermia and adjuvants develop a similar injury. The "mitochondrial" fraction of the testis of guinea pig is effective while repeated injections of alcoholic extract of testis emulsified with paraffin oil containing mycobacteria do not cause aspermatogenesis. The presence of acid-fast bacilli in the water-in-oil emulsion containing testis or spermia seems to be essential for the production of testicular lesions; the injection of antigen and mycobacteria into different sites is ineffective. When guinea pig testis is replaced by guinea pig liver or kidney or rabbit testis no testicular damage occurs. The injection of rabbit spinal cord combined with adjuvants results in allergic encephalomyelitis in a large proportion of guinea pigs, accompanied by a great loss of weight. The testes of a few of these animals show a varying degree of aspermatogenesis. When guinea pig brain is combined with adjuvants and administered subcutaneously the incidence of testicular injury is high, although the damage is, in general, mild. From the standpoint of mechanism, the inhibition of spermatogenesis which occurs in these animals may be unrelated to the injury which follows the injection of germinal cells. Aspermatogenesis follows the injection of killed mycobacteria in paraffin oil into the testis as well as into certain sites related to the gonad: the abdominal cavity, the subcutaneous tissue over the abdomen, and the skin of the inguinal region. Antibodies fixing complement in the presence of spermia are demonstrable in the sera of guinea pigs injected with testis or spermia and adjuvants. When the mycobacteria are omitted the titers are low and no testicular injury occurs. Although there seems to be a correlation between testicular damage and complement-fixing titer, this may not be a causal relationship. Antibodies which neutralize guinea pig hyaluronidase and those which immobilize spermia have also been demonstrated in the sera of these guinea pigs.


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