Lipid peroxidation in rats administrated with mercuric chloride
Related Experiment Video
Updated: Nov 4, 2026
Inducing Acute Liver Injury in Rats via Carbon Tetrachloride (CCl4) Exposure Through an Orogastric Tube
Published on: April 28, 2020
Y L Huang1, S L Cheng, T H Lin
1School of Technology for Medical Sciences, Kaohsiung Medical College, Taiwan, R.O.C.
Abstract:
Parenteral administration of mercuric chloride (HgCl2) to rats enhanced lipid peroxidation in liver, kidney, lung, testis, and serum (but not in heart, spleen, or muscle), as measured by the thiobarbituric acid reaction for malondialdehyde (MDA) in fresh tissue homogenates and body fluids. After sc injection of HgCl2 (5 mg/kg body wt), MDA concentrations in liver and kidney became significantly increased by 9 h and reached peak values at 24 h. Dose-response studies were carried out with male albino rats of the Fisher-344 strain (body wt 170-280 g) injected with 1, 3, 5 mg Hg/kg as HgCl2 and sacrificed after 24 h. In time-response studies, animals were administered 5 mg Hg/kg as HgCl2 and sacrificed after 3, 9, 18, 24, and 48 h. Studies in the authors' laboratory have shown that (1) concentrations of MDA are increased in targets (liver, kidney, lung, and testis) of HgCl2-treated rats; (2) severity of hepatotoxicity and nephrotoxicity is generally consistent with the elevation of Hg and MDA concentrations, based upon the time-course and dose-effect relationships observed after administration of HgCl2 to rats; and (3) concentrations of MDA are reduced in target tissues after pre-treatment with antioxidants and chelators to HgCl2-treated rats. The results of this study implicate that the lipid peroxidation is one of the molecular mechanisms for cell injury in acute HgCl2 poisoning.
Insights
Mercuric chloride (HgCl2) exposure in rats significantly increases lipid peroxidation, measured as malondialdehyde (MDA), in vital organs like the liver and kidneys. This suggests lipid peroxidation is a key mechanism in acute mercury poisoning.
Area of Science:
- Toxicology
- Biochemistry
- Cellular Biology
Background:
- Mercuric chloride (HgCl2) is a known nephrotoxic and hepatotoxic agent.
- The precise molecular mechanisms underlying Hg2+ induced cellular injury are not fully elucidated.
Purpose of the Study:
- To investigate the role of lipid peroxidation in acute mercuric chloride (HgCl2) poisoning.
- To determine the time-course and dose-dependency of HgCl2-induced oxidative stress in rat tissues.
Main Methods:
- Parenteral administration of HgCl2 to male Fisher-344 rats at varying doses (1-5 mg/kg) and time points (3-48 hours).
- Quantification of malondialdehyde (MDA) levels, a marker of lipid peroxidation, in liver, kidney, lung, testis, heart, spleen, and muscle homogenates, as well as serum.
- Assessment of hepatotoxicity and nephrotoxicity in relation to Hg and MDA concentrations.
Main Results:
- HgCl2 administration significantly increased MDA concentrations in the liver, kidney, lung, and testis, with peak levels observed at 24 hours post-injection.
- MDA elevation in target organs correlated with the severity of observed hepatotoxicity and nephrotoxicity.
- Pre-treatment with antioxidants and chelators reduced MDA levels in HgCl2-treated rats.
Conclusions:
- Lipid peroxidation, evidenced by increased MDA, is implicated as a significant molecular mechanism contributing to cellular injury in acute mercuric chloride poisoning.
- The findings highlight the critical role of oxidative stress in mercury toxicity, providing a basis for potential therapeutic interventions.
