Cadmium-induced testicular injury

Cadmium-induced testicular injury

Autor Siu, Erica R. Google Scholar
Mruk, Dolores D. Google Scholar
Porto, Catarina S. Autor UNIFESP Google Scholar
Cheng, C. Yan Google Scholar
Instituição Populat Council
Universidade Federal de São Paulo (UNIFESP)
Resumo Cadmium (Cd) is an environmental toxicant and an endocrine disrupter in humans and rodents. Several organs (e.g., kidney, liver) are affected by Cd and recent studies have illustrated that the testis is exceedingly sensitive to Cd toxicity. More important, Cd and other toxicants, such as heavy metals (e.g., lead, mercury) and estrogenic-based compounds (e.g., bisphenols) may account for the recent declining fertility in men among developed countries by reducing sperm count and testis function. in this review, we critically discuss recent data in the field that have demonstrated the Cd-induced toxicity to the testis is probably the result of interactions of a complex network of causes. This is likely to involve the disruption of the blood-testis barrier (BTB) via specific signal transduction pathways and signaling molecules, such as p38 mitogen-activated protein kinase (MAPK). We also summarize current studies on factors that confer and/or regulate the testis sensitivity to Cd, such as Cd transporters and metallothioneins, the impact of Cd on the testis as an endocrine disruptor and oxidative stress inducer, and how it may disrupt the Zn(2+) and/or Ca(2+) mediated cellular events. While much work is needed before a unified mechanistic pathway of Cd-induced testicular toxicity emerges, recent studies have helped to identify some of the likely mechanisms and/or events that take place during Cd-induced testis injury. Furthermore, some of the recent studies have shed lights on potential therapeutic or preventive approaches that can be developed in future studies by blocking or minimizing the destructive effects of Cd to testicular function in men. (C) 2009 Elsevier Inc. All rights reserved
Assunto Environmental toxicant
Seminiferous epithelial cycle
Sertoli cells
Germ cells
Blood-testis barrier
Cell adhesion
Idioma Inglês
Financiador National Institutes of Health
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Número do financiamento National Institutes of Health: R01 HD056034
National Institutes of Health: R03 HD051512
National Institutes of Health: U54 HD029990
FAPESP: 06/51281-6
Data 2009-08-01
Publicado em Toxicology and Applied Pharmacology. San Diego: Academic Press Inc Elsevier Science, v. 238, n. 3, p. 240-249, 2009.
ISSN 0041-008X (Sherpa/Romeo, fator de impacto)
Editor Elsevier B.V.
Extensão 240-249
Direito de acesso Acesso restrito
Tipo Resenha
Web of Science WOS:000268147600007

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