Publication: Epigallocatechin-3-gallate protects the testis from damage generated by experimental cryptorchidism in rabbits
Authors
Vigueras Villaseñor, Rosa María ; Jiménez Cabrera, Tania ; Chávez Saldaña, Margarita ; Jiménez Trejo, Francisco ; Cuevas Alpuche, Osvaldo ; Rojas Castañeda, Julio César
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Publisher
Universidad de Murcia. Departamento de Biología Celular e Histología
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DOI
DOI: 10.14670/HH-18-096
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info:eu-repo/semantics/article
Description
Abstract
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 17β-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.
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Citation
Histology and Histopathology, Vol.34, nº8, (2019)
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