Epicatechin ameliorates glucose intolerance and hepatotoxicity in sodium arsenite-treated mice.

in Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association by Sara Hejazi, Mehrnoosh Moosavi, Shahrzad Molavinia, Esrafil Mansouri, Reza Azadnasab, Mohammad Javad Khodayar

TLDR

  • This study found that a natural compound called epicatechin (EC) can help protect the liver from damage caused by a toxic substance called sodium arsenite (SA). The study used mice as a model organism and found that EC can improve glucose metabolism in mice. The study's findings suggest that EC could be used as a potential treatment for SA-induced liver toxicity and GI in humans.

Abstract

Arsenic is a metalloid found in the environment that causes toxic effects in different organs, mainly the liver. This study aimed to investigate the protective effects of epicatechin (EC), a natural flavonol, on glucose intolerance (GI) and liver toxicity caused by sodium arsenite (SA) in mice. Our findings showed that SA exposure led to the development of GI. Liver tissue damage and decreased pancreatic Langerhans islet size were also observed in this study. Mice exposed to sodium arsenite (SA) exhibited hepatic oxidative damage, indicated by reduced antioxidant markers (such as superoxide dismutase, catalase, glutathione peroxidase, and glutathione), along with elevated levels of thiobarbituric acid reactive substances. SA administration elevated the serum activities of liver enzymes alanine aminotransferase, aspartate transaminase, and alkaline phosphatase. Furthermore, notable increases in the levels of inflammatory and apoptotic markers (Toll-like receptor 4, nuclear factor-kappa B, tumor necrosis factor-α, nitric oxide, B-cell lymphoma-2, and cysteine aspartate-specific protease-3) were observed in the liver. Treatment of SA-exposed mice with EC considerably reversed these biochemical and histological changes. This study demonstrated the beneficial effects of EC in ameliorating SA-induced hyperglycemia and hepatotoxicity due to its ability to enhance the antioxidant system by modulating inflammation and apoptosis.

Overview

  • The study investigates the protective effects of epicatechin (EC) on glucose intolerance (GI) and liver toxicity caused by sodium arsenite (SA) in mice. The hypothesis being tested is whether EC can ameliorate the toxic effects of SA on the liver and improve glucose metabolism in mice. The methodology used for the experiment includes exposing mice to SA and EC, and measuring various biochemical and histological parameters such as liver enzymes, antioxidant markers, inflammatory and apoptotic markers, and glucose metabolism. The primary objective of the study is to determine the protective effects of EC on SA-induced liver toxicity and GI in mice.

Comparative Analysis & Findings

  • The study found that SA exposure led to the development of GI, liver tissue damage, and decreased pancreatic Langerhans islet size in mice. SA administration elevated the serum activities of liver enzymes alanine aminotransferase, aspartate transaminase, and alkaline phosphatase, and notable increases in the levels of inflammatory and apoptotic markers (Toll-like receptor 4, nuclear factor-kappa B, tumor necrosis factor-α, nitric oxide, B-cell lymphoma-2, and cysteine aspartate-specific protease-3) were observed in the liver. Treatment of SA-exposed mice with EC significantly reversed these biochemical and histological changes, indicating the protective effects of EC on SA-induced liver toxicity and GI in mice.

Implications and Future Directions

  • The study's findings suggest that EC can ameliorate the toxic effects of SA on the liver and improve glucose metabolism in mice. The study's limitations include the use of mice as a model organism, which may not fully represent the effects of SA on humans. Future research should investigate the protective effects of EC on SA-induced liver toxicity and GI in humans. Additionally, further studies should explore the underlying mechanisms of EC's protective effects on the liver and glucose metabolism.
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