Effect of the CYP2E1 genotype on vinyl chloride monomer-induced liver fibrosis among polyvinyl chloride workers

Hsieh, Hui-I; Chen, Pau‐Chung; Wong, Ruey-Hong; Wang, Jung‐Der; Yang, Pei–Ming; Cheng, Tsun‐Jen

doi:10.1016/j.tox.2007.06.089

Cited by 19 publications

(15 citation statements)

References 37 publications

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“…DNA templates were amplified with the primers: 5-CTTCCACGCACATCCTCTTCC-3 (upstream) and 5-AAGCCCCTTTCTTT TTCAGC-3 (downstream). Briefly, for the CYP450 2E1 gene analysis (rs3813867), any RFLP was detected by differences in PstI sites in the 5-flanking region following PCR amplification, using methods described by Hayashi et al (1991) and Hsieh et al (2007). The primers used for the amplification of CYP2E1 gene were 5-CCA GTC GAG TCT ACA TTG TCA-3 and 5-TTC ATT CTG TCT TCT AAC TGG-3.…”

Section: Methodsmentioning

confidence: 99%

Association between polymorphism of GSTP1, GSTT1, GSTM1 and CYP2E1 genes and susceptibility to benzene-induced hematotoxicity

et al. 2017

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Occupational exposure to benzene has been associated with leukemia, anemia, leukopenia, and thrombocytopenia. Genetic susceptibility to benzene toxicity in humans may be related to variations in benzene metabolizing genes. The main objective of this study was to ascertain whether polymorphism of GSTP1, GSTM1, GSTT1 and CYP2E1 genes might influence susceptibility to the adverse effects of benzene among employees of a petrochemical plant. In this cross-sectional study, 124 employees of a petrochemical plant who had been occupationally exposed to benzene and had one or more abnormal hematological parameter (cases) and 184 subjects with a similar exposure scenario, free from any abnormal hematological parameters (referent) were studied. Atmospheric concentrations of benzene were measured and GSTM1 and GSTT1 genotypes were evaluated using the multiplex polymerase chain reaction (PCR) technique. Additionally, GSTP1 and CYP2E1 genotypes were determined by PCR- restriction fragment length polymorphism (PCR–RFLP). The frequency of null GSTT1 genotype in cases was significantly higher than that of referent group (32.3 vs. 18.5%, OR 2.1, 95% CI 1.23–3.56, p = 0.004). The mean value of platelets in subjects with null GSTT1 genotype was significantly lower than that of individuals with positive GSTT1 genotype (p = 0.015). Conversely, the mean value of leukocytes was significantly higher in subjects with null GSTM1 genotype as compared to those with positive GSTM1 genotype (p = 0.026). Logistic regression analysis showed that, subjects with null GSTT1 genotype had a significantly higher risk for hematological disorders, as compared to those with positive GSTT1 genotype (OR 2.1, 95% CI 1.23–3.56). Moreover, subjects with both null GSTT1 and GSTM1 genotypes had a significantly higher risk for hematological disorders as compared to subjects with positive GSTT1 and GSTM1 genotypes (OR 2.35, 95% CI 1.14–4.8). The results of this study showed that, individuals carrying null GSTT1 or both null STT1 and GSTM1 genotypes had a higher risk and were more susceptible to benzene-induced hematological disorders.

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Section: Methodsmentioning

confidence: 99%

Association between polymorphism of GSTP1, GSTT1, GSTM1 and CYP2E1 genes and susceptibility to benzene-induced hematotoxicity

et al. 2017

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“…At concentrations up to approximately 220 ppm, VC is metabolized by CYP2E1 forming the highly reactive genotoxic epoxide, chloroethylene oxide. CYP2E1 polymorphisms were associated with fibrosis, liver injury, and chromosomal damage in Asian VC workers and possibly hemangiosarcoma at the Louisville plant (Antonino-Green et al 2000; Hsieh et al 2007; Huang et al 1997; Ji et al 2011). Chloroethylene oxide is either spontaneously or enzymatically converted into chloroacetaldehyde (CAA).…”

Section: Chemical Exposures Associated With Tashmentioning

confidence: 99%

“…Occupational and environmental liver diseases may present with a wide clinical spectrum ranging from asymptomatic liver enzyme elevation to acute liver failure, cirrhosis, and cancer. In addition to the exposure level, an individual’s susceptibility to chemical-induced liver disease is determined by polymorphisms in the genes of xenobiotic metabolism, concomitant use of alcohol or prescription medications, nutritional factors, and obesity—as many organic chemicals are lipid soluble (Hsieh et al 2007; Mastrangelo et al 2004). High-level vinyl chloride (VC; Cave, Falkner, et al 2010) and solvent exposures (Brautbar and Williams 2002) have historically been associated with occupational liver disease, while classically described mediators of environmental liver disease include aflatoxins (Kensler et al 2011) analines (Epping Jaundice; Kopelman, Scheurer, and Williams 1966; Nichols 2004), and toxic oil syndrome (Gelpi et al 2002)).…”

Section: Introductionmentioning

confidence: 99%

Toxicant-associated Steatohepatitis

et al. 2012

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Hepatotoxicity is the most common organ injury due to occupational and environmental exposures to industrial chemicals. A wide range of liver pathologies ranging from necrosis to cancer have been observed following chemical exposures both in humans and in animal models. Toxicant-associated fatty liver disease (TAFLD) is a recently named form of liver injury pathologically similar to alcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD). Toxicant-associated steatohepatitis (TASH) is a more severe form of TAFLD characterized by hepatic steatosis, inflammatory infiltrate, and in some cases, fibrosis. While subjects with TASH have exposures to industrial chemicals, such as vinyl chloride, they do not have traditional risk factors for fatty liver such as significant alcohol consumption or obesity. Conventional biomarkers of hepatotoxicity including serum alanine aminotransferase activity may be normal in TASH, making screening problematic. This article examines selected chemical exposures associated with TAFLD in human subjects or animal models and concisely reviews the closely related NAFLD and ALD.

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“…Other polymorphisms in the Phase II VC metabolic pathway including ALDH2, GSTM1 and GSTT1 have also been implicated in modulating VC-induced DNA damage in some but not all VC worker populations. [3340–4750–54]…”

Section: The Molecular Epidemiology Of Vinyl Chloride Carcinogenesismentioning

confidence: 99%

Plastics and carcinogenesis: The example of vinyl chloride

Brandt‐Rauf¹,

Li²,

Long³

et al. 2012

J Carcinog

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The manufacture, use and disposal of various plastics can pose numerous health risks, including the risk of cancer. A model example of carcinogenic risk from plastics is provided by polyvinyl chloride, since it is composed of the known human carcinogen vinyl chloride (VC). In recent years, much has been learned about the molecular biological pathways of VC carcinogenesis. This has led to molecular epidemiologic studies of VC carcinogenesis in exposed human populations which have identified useful biomarkers of exposure, effect and susceptibility for VC. These studies have in turn provided the basis for new molecular approaches for the prevention and treatment of VC cancers. This model could have much wider applicability for many other carcinogenic exposures and many other human cancers.

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Effect of the CYP2E1 genotype on vinyl chloride monomer-induced liver fibrosis among polyvinyl chloride workers

Cited by 19 publications

References 37 publications

Association between polymorphism of GSTP1, GSTT1, GSTM1 and CYP2E1 genes and susceptibility to benzene-induced hematotoxicity

Association between polymorphism of GSTP1, GSTT1, GSTM1 and CYP2E1 genes and susceptibility to benzene-induced hematotoxicity

Toxicant-associated Steatohepatitis

Plastics and carcinogenesis: The example of vinyl chloride

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