2008
DOI: 10.1007/s12011-008-8234-4
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The Interactions between the Chronic Exposure to Aluminum and Liver Regeneration on Bile Flow and Organic Anion Transport in Rats

Abstract: The chronic exposure to Aluminum (Al) may compromise different liver functions, mainly during the hepatic regeneration. The aim of this study is to investigate the interactions between the chronic i.p. exposure to Al and hepatic regeneration (HR) on bile flow and organic anion transport in experimental animals. For this purpose, we studied bile flow and fractional transfer rates for the transport of hepatic organic anions (hepatic uptake, sinusoidal efflux, and canalicular excretion), as well as parameters rel… Show more

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Cited by 40 publications
(16 citation statements)
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“…DDT treatment downregulated Bax, up-regulated Bcl-2 expression, inhibited Bax translocation to mitochondria, restrained mitochondriamediated apoptotic pathways, inhibited the cleavage of caspase-3 and PARP, and inhibited the fragmentation of internucleosomal DNA to protect PC12 cells from apoptosis. In previous studies, the mechanism of Al toxicity has been poorly understood, but the literature has suggested that Al generates ROS that cause lipid peroxidation, oxidative damage to proteins and DNA, as well as decreased intracellular glutathione (González et al, 2009). As oxidative stress is an important factor in neuronal injury, we re-explored the conditions of oxidative-stress production and found that ROS production was increased most obviously at 6 h of Al exposure.…”
Section: Discussionmentioning
confidence: 95%
“…DDT treatment downregulated Bax, up-regulated Bcl-2 expression, inhibited Bax translocation to mitochondria, restrained mitochondriamediated apoptotic pathways, inhibited the cleavage of caspase-3 and PARP, and inhibited the fragmentation of internucleosomal DNA to protect PC12 cells from apoptosis. In previous studies, the mechanism of Al toxicity has been poorly understood, but the literature has suggested that Al generates ROS that cause lipid peroxidation, oxidative damage to proteins and DNA, as well as decreased intracellular glutathione (González et al, 2009). As oxidative stress is an important factor in neuronal injury, we re-explored the conditions of oxidative-stress production and found that ROS production was increased most obviously at 6 h of Al exposure.…”
Section: Discussionmentioning
confidence: 95%
“…Al sources are mainly corn, yellow cheese, salt, herbs, spices, tea, cosmetics, ware, and containers. It has been reported that Al could accumulate in all tissues of animals, preferentially in liver, heart, bones and brain (2). This metal disrupts the prooxidant/antioxidant balance in tissues leading to biochemical and physiological dysfunction due to an excessive reactive oxygen species (ROS) generation (3,4).…”
Section: Introductionmentioning
confidence: 99%
“…The mechanism of Al toxicity is poorly understood, but the literature suggests that Al generates reactive oxygen species (ROS) that cause lipid peroxidation (LPO) and oxidative damage to proteins and DNA and decreases intracellular glutathione (GSH) (González et al . ). To control the level of ROS and to protect cells under stress conditions, mammalian tissues contain several enzymes that scavenge ROS such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S‐transferase (GST) and GSH (Dkhil et al .…”
mentioning
confidence: 97%