Abstract
Benzene is a well-known hematotoxic carcinogen that can cause leukemia and a variety of blood disorders. Our previous study indicated that benzene disturbs levels of metabolites in the fatty acid β-oxidation (FAO) pathway, which is crucial for the maintenance and function of hematopoietic and leukemic cells. The present research aims to investigate the effects of benzene on changes in the expression of key enzymes in the FAO pathway in male C3H/He mice. Results showed that benzene exposure caused reduced peripheral white blood cell (WBC), red blood cell (RBC), platelet (Pit) counts, and hemoglobin (Hgb) concentration. Investigation of the effects of benzene on the expression of FA transport- and β-oxidation-related enzymes showed that expression of proteins Cpt1a, Crat, Acaa2, Aldh1l2, Acadvl, Crot, Echs1, and Hadha was significantly increased. The ATP levels and mitochondrial membrane potential decreased in mice exposed to benzene. Meanwhile, reactive oxygen species (ROS), hydrogen peroxide (H2O2), and malondialdehyde (MDA) levels were significantly increased in the benzene group. Our results indicate that benzene induces increased expression of FA transport and β-oxidation enzymes, mitochondrial dysfunction, and oxidative stress, which may play a role in benzene-induced hematotoxicity.
Highlights
Benzene is a ubiquitous environmental and occupational pollutant
We examine the effects of benzene on the expression of key enzymes in the fatty acid β-oxidation (FAO) pathway, as well as its effects on mitochondrial function and oxidative stress
The results showed that the protein levels of acyltransferase 2 (Acaa2), Aldh1l2, Acadvl, Aldh1l2, Acadvl, carnitine O-octanoyltransferase (Crot), enoyl coenzyme A hydratase short chain 1 (Echs1), and
Summary
Benzene is a ubiquitous environmental and occupational pollutant. It is a recognized cause of acute myeloid leukemia and acute non-lymphocytic leukemia [1,2,3]. Studies showed that benzene causes hematotoxic effects, even at exposure levels lower than 1 ppm [4,5,6]. Many epidemiological and experimental studies have been carried out, the mechanisms of benzene-induced hematotoxicity remain to be elucidated. Recent studies demonstrated that fatty acid β-oxidation (FAO) is a crucial pathway for HSCs and leukemic cells. Ito et al reported that inhibition of FAO results in the symmetric commitment of HSC
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