Stem cell and benzene-induced malignancy and hematotoxicity.

Abstract

The biological effect of benzene on the hematopoietic system has been known for over a century. The rapid advancement in understanding the biology of hematopoietic stem cells (HSCs) and cancer stem cells (CSCs) in recent years has renewed interest in investigating the role of stem cells in benzene-induced malignancy and bone marrow depression. The interplay between benzene and stem cells is complex involving the stem cell, progenitor, and HSC niche compartments of the bone marrow. In this prospect, benzene metabolites formed through metabolism in the liver and bone marrow cause damage in hematopoietic cells via multiple mechanisms that, in addition to traditionally recognized chromosomal aberration and covalent binding, incorporate oxidative stress, alteration of gene expression, apoptosis, error-prone DNA repair, epigenetic regulation, and disruption of tumor surveillance. However, benzene-exposed individuals exhibit variable susceptibility to benzene effect that arises, in part, from genetic variations in benzene metabolism, DNA repair, genomic stability, and immune function. These new studies of benzene leukemogenesis and hematotoxicity are expected to provide insights into how environmental and occupational chemicals affect stem cells to cause cancer and toxicity, which impact the risk assessment, permissible level, and therapy of benzene exposure.

• Authors: Liping Wang, Xiaoqing He, Yongyi Bi, Qiang Ma
• Journal: Chemical research in toxicology (Chem Res Toxicol) Vol. 25 Issue 7 Pg. 1303-15 (Jul 16 2012) ISSN: 1520-5010 [Electronic] United States
• PMID: 22540379 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., Review)

Chemical References

• Receptors, Aryl Hydrocarbon
• Benzene

Topics

• Apoptosis (drug effects)
• Benzene (chemistry, toxicity)
• Bone Marrow Cells (drug effects, metabolism)
• DNA Repair
• Epigenesis, Genetic (drug effects)
• Hematopoietic Stem Cells (metabolism)
• Humans
• Immunosuppression Therapy
• Leukemia (chemically induced, metabolism, pathology)
• Neoplastic Stem Cells (metabolism)
• Oxidative Stress (drug effects)
• Receptors, Aryl Hydrocarbon (chemistry, metabolism)