Pesticides Drive Liver Diseases Through Non-Apoptotic Regulated Cell Death Pathways

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Authors: Zamza Khairullina, Saulesh S. Kurmangaliyeva, Rustam Yussupov, Elmira Kelimberdiyeva, Liliya Tryfonyuk, Nasriddin Shapambayev, Aizat Seidakhmetova, Talgat Medetbekov, Anton Tkachenko
Cited by: 1
References: 273

Abstract

A compelling body of evidence links pesticide exposure to human diseases. The liver plays a central role in the detoxification of pesticides, suggesting intense pesticide-liver cell interactions. A growing body of studies highlighted in this review supports the contribution of pesticides of various chemical classes to the development of non-alcoholic fatty liver disease (NAFLD), alcohol-associated liver disease (ALD), liver cirrhosis, viral hepatitis, hepatocellular carcinoma, etc., via disrupting lipid and carbohydrate metabolism and redox homeostasis, promoting endoplasmic reticulum stress and mitochondrial dysfunction, as well as stimulating apoptosis, fibrosis, and inflammation. In this review, we systematically illustrated an underappreciated mechanism of pesticide-induced overall and hepatic toxicity, i.e., the ability to induce non-apoptotic regulated cell death (RCD) pathways such as ferroptosis, necroptosis, and pyroptosis. Our analysis indicates that pesticides are implicated in driving liver diseases by inducing ferroptosis, necroptosis, and pyroptosis. Non-apoptotic RCDs mediate pesticide-induced liver steatosis and fibrosis. Furthermore, these cell death modalities fuel inflammation through the promotion of pro-inflammatory cytokine production and the generation of damage-associated molecular patterns. Understanding of deeper mechanisms of pesticide-induced effects on the non-apoptotic cell death machinery and subsequent immunogenic effects in liver pathology might help develop novel preventive strategies to reduce liver damage.

Fields of Study & Subjects

Pesticide Exposure and Toxicity Paraquat toxicity studies and treatments Drug-Induced Hepatotoxicity and Protection

Publication details

Journal / source
Diseases
Publisher
MDPI AG
Volume
14
Issue
3
Pages
96–96
Publication date
5 March 2026
Language
EN