The overlooked impact of cadmium on the progression of chronic hepatitis and the onset of renal failure in advanced cirrhosis.

Autor: Cirovic A; Faculty of Medicine, Institute of Anatomy, University of Belgrade, Dr Subotica 4/2, Belgrade 11000, Serbia., Satarug S; Kidney Disease Research Collaborative, Translational Research Institute, Woolloongabba, Brisbane, QLD 4102, Australia. Electronic address: sj.satarug@yahoo.com.au., Jevtic J; Faculty of Medicine, Institute of Pathology, University of Belgrade, Dr Subotica 1, Belgrade 11000, Serbia., Ivanovski A; Faculty of Medicine, University of Belgrade, Dr Subotica 4/2, Belgrade 11000, Serbia., Orisakwe OE; African Centre of Excellence for Public Health and Toxicological Research (ACE-PUTOR), University of Port Harcourt, PMB, Choba, Port Harcourt 5323, Nigeria; Advanced Research Centre, European University of Lefke, Lefke, Northern Cyprus, TR-10, Mersin, Turkey., Jankovic S; Institute of Meat Hygiene and Technology, Kacanskog 13, Belgrade 11040, Serbia., Cirovic A; Faculty of Medicine, Institute of Anatomy, University of Belgrade, Dr Subotica 4/2, Belgrade 11000, Serbia. Electronic address: aleksandar.cirovic.7@gmail.com.
Jazyk: angličtina
Zdroj: Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) [J Trace Elem Med Biol] 2024 Dec; Vol. 86, pp. 127542. Date of Electronic Publication: 2024 Oct 06.
DOI: 10.1016/j.jtemb.2024.127542
Abstrakt: The mechanism of hepatocyte destruction in chronic hepatitis is not completely understood, while renal failure in individuals with advanced cirrhosis is a significant concern. It is well known that smokers who are chronically infected with hepatitis B and C viruses (HBV, HCV) have a poor prognosis. In the present review, we propose a novel hypothesis that environmental exposure to a nephrotoxic metal pollutant, cadmium (Cd) may contribute to hepatocyte destruction and, subsequently, affect the duration of chronic hepatitis. The metal binding protein, metallothionein (MT) sequesters cadmium as CdMT complexes, and effectively neutralize its adverse effects. Cadmium can cause the damage to hepatocytes, only when it is in an unbound form. In addition to its ability to bind cadmium, MT can act as a scavenger of reactive oxygen species (ROS). However, the cellular MT levels may decrease, when ROS is excessively produced under the pathologic chronic viral hepatitis conditions, especially while the cellular levels of zinc may also be low. Zinc is an endogenous inducer of MT, and is required for maximal MT expression. High ROS levels in the hepatocytes diminishes MT binding to metals. Consequently, the proportion of unbound Cd is increased and thus there is more hepatic damage. Hepatic damage leads to a copious release of CdMT into the circulation. This significant cadmium load, which occurs after hepatic damage, and in some cases, muscle atrophy, induces kidney damage with resultant renal failure in advanced cirrhosis.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier GmbH. All rights reserved.)
Databáze: MEDLINE
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