Chemically and pharmacologically induced liver toxicity models in experimental animals and observed changes

Chemically and pharmacologically induced liver toxicity models

Abstract

Toxicity models conducted using laboratory animals are widely preferred in biomedical research to understand the effects of toxic substances on biological systems, to make safety assessments, and to test therapeutic approaches. Another reason is the physiological and anatomical similarities of mice, rats, and rabbits to humans. Although there are many experimental liver toxicity models, toxicity models created with drugs and chemicals are preferred over surgical models. These models aim to simulate many conditions such as acute or chronic toxicities, drug toxicities, hepatitis, steatosis, and cirrhosis. Toxicology models have a special importance because the liver is considered one of the most vulnerable organs to toxic substances due to its metabolic functions. In this context, experimental toxicity models created with many drugs and chemicals such as acetaminophen, cadmium, ethanol, carbon tetrachloride, and diclofenac have been evaluated. In experimental studies, although different among models, biochemically elevated alanine aminotransferase (ALT), aspartate aminotransferase (AST), and malondialdehyde (MDA) levels indicate liver damage, while decreased glutathione (GSH) levels reflect weakened antioxidant defenses. Histopathologically, although different among models, necrosis, fibrosis, fat accumulation and inflammation have been observed, depending on the type of toxin. Experimental liver toxicity models are indispensable for understanding liver pathophysiology, identifying potential risks and advancing hepatoprotective therapies. Their findings will improve biomedical research and clinical practice in addressing toxin-induced liver damage.