Exposure of Tg.AC transgenic mice to benzene suppresses hematopoietic progenitor cells and alters gene expression in critical signaling pathways

Comparison of Toxicity of Benzene Metabolite Hydroquinone in Hematopoietic Stem Cells Derived from Murine Embryonic Yolk Sac and Adult Bone Marrow

“…It is also used as an alternative method to animal models for the evaluation of the efficacy or lineage-specific toxicity of drugs and environmental chemicals on human and animal hematopoietic cells [49]. Studies have found that benzene exposure suppresses hematopoietic progenitor cell differentiation of multilineage colony forming unit (CFU-GEMM), colony forming unit (CFU-GM) and blast forming unit (BFUE/CFUE) in mice [50]. Hydroquinone exposure results in lineage-specific toxicities in both bone marrow and yolk sac hematopoietic stem cells by the CFC assay.…”

Lineage-related cytotoxicity and clonogenic profile of 1,4-benzoquinone-exposed hematopoietic stem and progenitor cells

“…For example, benzene reduced mouse BMderived CFU-S and GM-CFU-C (Green et al, 1981); benzene inhalation in mice reduced BM CFU-C (Toft et al, 1982); phenol, HQ, CT, 1,4-BQ, and trans,trans-muconic acid (TTMA) caused toxicity in mouse CFU-E, BFU-E, and CFU-C (Seidel et al, 1991); benzene inhalation in mice diminished the clonal capacity for BFU-E and CFU-GM (Abraham, 1996); phenol, HQ, CT, 1,4-BQ, and TTMA showed gender-and age-specific cytotoxic effects on mouse CFU-E (Corti and Snyder, 1998); and benzene exposure was found to suppress hematopoietic progenitor cell differentiation of CFU-GEMM, CFU-GM, and BFU-E/CFU-E in mice (Nwosu et al, 2004). The strength of the toxic effects of 1,4-BQ in our study was comprehensively evaluated for all types of progenitor colony formation (single-lineage: CFU-E, BFU-E, CFU-G, and CFU-M; multi-lineage: CFU-GM and CFU-GEMM).…”

Bone Marrow Stem Cells and Genotoxicity Studies in These Cells: Review

“…tarafından yapılan çalışmalarda da benzen detoksikasyonunda görev alan kinon oksidoredüktaz-1 ve mikrozomal epoksit redüktaz enzimlerinin hematotoksisite ve genotoksisite oluşumunda belirleyici oldukları görülmüştür. 64,65 İnhalasyon yolu ile benzene maruz bırakılan farelerdeki hematopoietik kök hücre ve kemik iliği incelemesinde ise, benzenin kemik iliği hücrelerinde p21 mRNA indüksiyonu yaparken hematopoietik kök hücrelerde değişikliğe neden olmadığı, fankoni anemisindeki DNA hasar mekanizmasında da p53/p21 hiperaktivasyonunun sorumlu olduğu belirlenmiştir. 66,67 Zhang ve ark.…”