Liver and Cadmium ToxicityVerónica Souza Arroyo, Karina Martínez Flores, Leticia Bucio Ortiz, Luis Enrique Gómez-Quiroz and María Concepción Gutiérrez-Ruiz*
Laboratorio de Fisiología Celular, Departamento de Ciencias de la Salud, División de Ciencias Biológicas y de la Salud. Universidad Autónoma Metropolitana-Iztapalapa, Avenida San Rafael Atlixco 186, Colonia Vicentina, México, D.F. 09340, México
- *Corresponding Author:
- Ma. Concepción Gutiérrez-Ruiz
Universidad Autónoma Metropolitana-Iztapalapa
Laboratorio de Fisiología Celular
Departamento de Ciencias de la Salud
División de Ciencias Biológicas y de la Salud
Avenida San Rafael Atlixco 186
México, D.F. 09340, México.
Fax: 52-55- 58044730
E-mail: [email protected]
Received Date: November 18, 2011; Accepted Date: December 27, 2011; Published Date: January 02, 2012
Citation: Arroyo VS, Flores KM, Ortiz LB, Gómez-Quiroz LE, Gutiérrez-Ruiz MC (2012) Liver and Cadmium Toxicity. J Drug Metabol Toxicol S5:001. doi: 10.4172/2157-7609.S5-001
Copyright: © 2012 Arroyo VS, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Cadmium (Cd) is an important environmental pollutant. This metal presents a serious threat for both, humans and animals health. The environmental risk can lead to the absorption of large quantities of Cd and its toxic action on the organism. It adversely affects some organs in humans and animals, including the liver, kidneys, lungs, pancreas, and testis. The liver and kidneys, which are the primary organs involved in the elimination of this metal, are especially sensitive to its toxic effects. The liver is the main target organ of Cd toxicity following both acute and chronic exposure. This review presents the current state of knowledge related to the cellular mechanisms of Cd toxicity in the liver. Different mechanisms are discussed: the disruption of the cellular antioxidant system and the decrease in thiol status, the generation of reactive oxygen species and oxidative stress, the interference of biological metal homeostasis, involvement of inflammatory mediators, disruption of cell adhesion and cell damage leading to apoptosis.