RESUMO
Cryptorchidism (CO) is a risk factor for infertility in men. It is associated with an increase in oxidative stress which alters the differentiation of the gonocytes to spermatogonia. Epigallocatechin-3-gallate (EGCG) is an antioxidant that acts as a free radical scavenger and activates the antioxidant enzymes. The aim of this work was to investigate if EGCG plays a role in the protection of the testicle from alterations generated by CO and its possible mechanism. Male rabbits 7 days old were divided into four groups and distributed as follows: 1) control (C) treated with EGCG vehicle (V) (C/V); 2) C with administration of EGCG from 65 to 120 days postpartum (dpp) (C/EGCG); 3) CO induced by administration of 17ß-estradiol plus EGCG vehicle (CO/V) and 4) CO plus EGCG administration (CO/EGCG). The animals were euthanized at 120 dpp and their testes were processed to evaluate lipid peroxidation, activities of superoxide dismutase (SOD) and catalase (CAT) enzymes as well as serum testosterone (T) concentrations. In addition, the rates of apoptosis, cell proliferation and histological alterations were determined. The CO/EGCG group showed a significant reduction in lipid peroxidation, a significant increase in the anti-oxidant enzyme activities and concentrations of T. Also, there was a significant decrease in the histological alterations, absence of gonocytes and active spermatogenesis when compared with CO/V group. These results show that EGCG reduces lipid peroxidation and increases the activity of the endogenous anti-oxidant system which protects the testes from alterations produced by oxidative stress generated during experimental CO.
Assuntos
Antioxidantes/farmacologia , Catequina/análogos & derivados , Criptorquidismo/tratamento farmacológico , Testículo/efeitos dos fármacos , Animais , Antioxidantes/uso terapêutico , Apoptose/efeitos dos fármacos , Catalase/metabolismo , Catequina/farmacologia , Catequina/uso terapêutico , Estradiol , Imuno-Histoquímica , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Estresse Oxidativo/efeitos dos fármacos , Coelhos , Superóxido Dismutase/metabolismo , Testículo/metabolismo , Testículo/patologiaRESUMO
Cryptorchidism causes apoptosis of germ cells. It has been suggested that the redox regulatory system is involved in this process. The free radicals produced are thought to be generated during the production of uric acid, a reaction catalyzed by xanthine oxidase. This enzyme is inhibited by allopurinol; however, the role of allopurinol in neonate rats with inguinal cryptorchidism has not been assessed yet. Sixty male Wistar rats were used and five groups were formed: a control, a sham, a sham group with allopurinol administration and two groups with surgical unilateral cryptorchidism, which either did not receive, or received, allopurinol. The rats were assessed at 40 days post-partum. Reactive oxygen species concentration and epithelial area were measured and the histopathological, apoptotic and cellular proliferation indexes were determined. We found a decrease in reactive oxygen species, histopathological and apoptotic indexes and an increase in proliferation index and epithelial area in rats with cryptorchidism treated with allopurinol in comparison with rats with untreated cryptorchidism. We suggest that the over-production of reactive oxygen species plays an important role in the damage of the cryptorchid testes. Allopurinol administration decreases reactive oxygen species concentrations as well as the damage to the germ epithelium.