Changes In Testes Of Rats Research Articles

The influence of hollyhock extract administration on testicular function in rats

It has been reported, recently that an aqueous extract from hollyhock flowers (Althaea rosea Cav. varietas nigra) induces weak metabolic changes in rat testes. In the present study, the in vivoinfluence of a methanolic extract was investigated on the metabolism and morphology of the rat testis. To this end, histochemical, morphometric and radioimmunological methods were used. The rats drank the extract at a dose of 100 mg/day for 7 weeks. The histochemical activities of glucose-6-phosphate dehydrogenase (G6PDH) and Delta(5)beta-hydroxysteroid dehydrogenase (Delta(5)betaHSD) increased significantly statistically in the Leydig cells of the experimental rats in comparison with controls. There were no significant changes in either the diameter of seminiferous tubules or the height of seminiferous epithelium after hollyhock administration. Further, only a small amount of hyperplasia of the interstitial tissue was observed. The morphological and histoenzymatic changes in the Leydig cells indicate that the methanolic hollyhock extract has a direct but small influence on rat testes. The insignificant changes in testicular testosterone and estradiol content suggest that the extract does not disturb steroidogenesis.

Evaluation of Chronic Exposure of the Male Rat Reproductive System to the Insecticide Methomyl

Carbamate insecticides are widely used in industry, agriculture and for public health purposes. Numerous incidents of acute carbamate poisoning have resulted from inhalation of sprays or contamination of crops or food. This work was conducted to study the effect of chronic exposure to methomyl on hormonal, histopathological and histochemical changes in rat testes. The treated group received methomyl orally (17 mg kg−1in saline) daily for 2 months, while the control group received saline. A significant decrease in the level of testosterone was observed in the intoxicated animals, while the levels of FSH, LH and prolactin were significantly increased. Histopathological studies of the intoxicated rat testes revealed variable degrees of degenerative changes in the seminiferous tubules up to total cellular destruction. As regards the histochemical results, it was found that both acid phosphatase and alpha esterase enzyme activity was significantly increased compared to the control group. On the other hand succinic dehydrogenase enzyme activity was significantly reduced. No significant change was observed in alkaline phosphatase enzyme activity. The hormonal changes and testicular damage continued for 30 days after withdrawal of the insecticide indicating a persistent effect. From the above-mentioned findings, it has been concluded that chronic exposure to methomyl insecticide has deleterious effects on rat testes. Therefore application of such insecticide should be limited to a designed program with special care in handling to limit or minimize its hazards.

Nitric oxide as a bifunctional regulator of apoptosis.

It was inevitable that important relationships between two of the most intensely studied topics in biomedical research, apoptosis and nitric oxide (NO), would become apparent. Apoptosis is essential to normal development as well as physiological cell turnover. Although apoptosis in excess can manifest as tissue damage, a failure to undergo apoptosis constitutes pathological cellular overgrowth. It is now evident that NO and its reaction products can either promote or prevent apoptosis in a multitude of settings. The ubiquitous distribution of the NO synthases and the remarkable diffusibility and diverse chemical reactivity of NO in biological systems make this molecule unique among the regulators of apoptosis. Understanding the factors that govern the consequences of NO exposure on cell viability and identifying the conditions in which NO regulation of apoptosis contribute to pathology are topics of considerable interest and potential importance. In this article, we will review the recent observations on NO as a regulator of apoptosis. Apoptosis, or programmed cell death, is distinguished from lytic or necrotic cell death by specific biochemical and structural events (see recent review in Reference 11 ). Apoptogenic signals trigger cell-specific signaling pathways, including protease activation, followed by the appearance of morphological changes characteristic of cells undergoing apoptosis, including condensation of nuclei and cytoplasm, blebbing of the cytoplasmic membranes, and finally fragmentation into apoptotic bodies that are phagocytosed by neighboring cells. The elucidation of the signaling events in apoptosis is occurring at a rapid pace and includes the identification of the key roles of cysteine proteases (known as caspases), Bcl-2 family members, and mitochondria. Caspases, the mammalian counterpart of ced-3 in Caenorhabditis elegans , are a family of cysteine proteases now known to contain at least 14 homologs. Ectopic expression of any of the caspase family proteases can cause apoptosis; however, not all caspase family …

Reversibility of testicular atrophy induced by di(2-ethylhexyl) phthalate in rats

Previous studies have shown that di(2-ethylhexyl) phthalate (DEHP) results in atrophy of testes and accessory sex organs accompanied by a decreased testicular concentration of zinc in rats. An experiment was performed to determine whether those changes in rat testes are reversible changes. Young Wistar male rats were administered 2.0 g/kg of DEHP for 14 days. At that time, one-half of the rats were killed for determination of zinc and testosterone concentrations in the testis, liver, and serum, and organ weights. The remaining rats were maintained for additional 45 days without further DEHP administration. Testicular weight of rats administered DEHP over the 14-day period was significantly less than that of the control animals, and testicular testosterone content and zinc concentrations were less than those of the control animals. At the end of the 45-day recovery phase, serum testosterone concentration returned to the control level, but testicular zinc concentration and testosterone content were still lower than those of the control animals. In addition, testicular weight of DEHP-treated rats was lower than that of the control animals and histologically, only a small number of seminiferous tubules showed spermatogenesis. These results indicate that, morphologically, DEHP-induced testicular atrophy appears to be of limited reversibility.

Effects of several anti-inflammatory drugs on cadmium-induced inflammation in rat testis

To investigate the effect of several anti-inflammatory drugs on cadmium-induced inflammation in the testis of rat, the degree of intratesticular hemorrhage and lipoperoxide level in the testis were measured as a parameter of the inflammation. Alpha-tocopherol and coenzyme Q10which are well known as antioxidative agents had a potent antiinflammatory effect on cadmium-induced inflammation in rat testis. On the other hand, indomethacin and peonol which are supposed to be potent inhibitors of cyclooxygenase activity and prostaglandin synthesis, enhanced cadmium-induced intratesticular hemorrhage in a dose dependent manner. As for glucocorticoid (predonin) which has been reported to be an inhibitory protein on phospholipase A2activity, a moderate inhibitory effect on inflammatory changes in rat testis induced by cadmium was observed although it was statistically not significant. These results suggest that oxidative and inflammatory reaction induced by cadmium in rat testis may be considered not to be promoted by the accerelation of cyclooxygenase pathway in arachidonic acid cascade, but by the accerelation of lipoxygenase pathway or radical reaction mediated oxygenation of nonesterified polyunsaturated fatty acids, which has been reported to be increased in the inflammation in the testis of rat induced by cadmium.

Effects of continuous administration of dietary theobromine on rat testicular weight and morphology

Previous studies have shown that high dietary theobromine levels fed to rats results in testicular atrophy with changes in testicular cytology. An experiment was performed to determine whether these changes in rat testes are reversible. Proven breeder male rats were fed Purina lab chow containing 0, 0.2, 0.6, or 0.8% theobromine for 49 days. At that time, unilateral orchiectomy was performed on all rats. Testicular weights in the rats fed 0.6 and 0.8% theobromine-containing diets were significantly less than those from control rats and from rats fed 0.2% dietary theobromine ( p < 0.01). The seminiferous tubules from rats fed the 0.6 or 0.8% theobromine diets showed extensive severe cellular degeneration and necrosis and contained many multinucleated cells. The interstitial tissue was edematous and there was evidence of apparent proliferation of arterioles. The rats were allowed to recover and were fed the diet without theobromine for an additional 49 days. Testicular weights of the rats given 0.6 and 0.8% dietary theobromine in the first 49-day period remained significantly below those of control rats and of rats fed 0.2% dietary theobromine ( p < 0.01). Histologically, 70 to 90% of the seminiferous tubules from the rats given the two highest dietary levels of theobromine appeared almost deplete of well-formed spermatozoa. These results indicate that the theobromine-induced testicular injury appears to be irreversible over time in the affected seminiferous tubules.

363. Steroid induced histological and biochemical changes in rat testis

363. Steroid induced histological and biochemical changes in rat testis