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Updated: Feb 7, 2026
10:56
A Familial Hypercholesterolemia Human Liver Chimeric Mouse Model Using Induced Pluripotent Stem Cell-derived Hepatocytes
Published on: September 15, 2018
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THE STATE OF THE CYSTATHIONINE GAMMA-LYASE / H2S SYSTEM IN THE LIVER AND SKELETAL MUSCLES OF RATS WITH
N Voloshchuk1, A Melnik1, O Danchenko1
1National Pirogov Memorial Medical University, Vinnytsia, Ukraine.
Georgian Medical News
|July 24, 2018
Summary
Simvastatin reduces hydrogen sulfide (H2S) production in rats, potentially causing liver and muscle damage. Propargylglycine (PAG) partially reversed this H2S deficiency but increased toxicity markers.
Area of Science:
- Biochemistry
- Pharmacology
- Toxicology
Background:
- Hypercholesterolemia is a risk factor for cardiovascular diseases.
- Statins, like simvastatin, are widely used to manage hypercholesterolemia.
- Hepatotoxicity and myotoxicity are known side effects of statin therapy.
Purpose of the Study:
- To investigate the impact of simvastatin on hydrogen sulfide (H2S) levels and cystathionine γ-lyase (CSE) activity in rat liver and skeletal muscles.
- To evaluate the role of propargylglycine (PAG) in mitigating simvastatin-induced hepato- and myotoxicity.
- To explore the potential link between H2S deficiency and simvastatin's adverse effects.
Main Methods:
- Studies were conducted on 94 male Wistar rats.
- Assessed H2S content and CSE activity in liver and skeletal muscles.
- Administered simvastatin and propargylglycine (PAG) to induce and modulate toxicity.
- Monitored serum markers of cytolysis.
Main Results:
- Simvastatin treatment inhibited CSE-mediated H2S synthesis in target organs, negatively impacting their biochemical and functional status.
- PAG administration partially reversed simvastatin-induced H2S deficiency.
- PAG treatment was associated with increased serum cytolysis markers, correlating negatively with CSE activity and H2S levels in organs.
Conclusions:
- Simvastatin-induced H2S deficiency is a likely molecular mechanism underlying its hepato- and myotoxicity.
- Targeting H2S metabolism may offer a strategy to reduce statin-associated side effects.
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