Glutathione S-Transferases GSTM1 and GSTT1 Polymorphisms and Asbestosis

Franko, Alenka; Dodic-Fikfak, Metoda; Arnerić, Niko; Dolžan, Vita

doi:10.1097/jom.0b013e318065b855

Cited by 22 publications

(31 citation statements)

References 31 publications

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“…Important findings of our previous studies show that the GSTT1-null genotype, which results in the absence of an active enzyme, as well as the GSTP1 genotype coding for an enzyme with high conjugation capacity, were associated with an increased risk of asbestosis (7,31). In line with these reports, the results of this study, although statistically insignificant, could support the hypothesis that genetic polymorphisms of metabolic enzymes play an important role in the development of asbestosis.…”

Section: Discussionsupporting

confidence: 81%

“…No significant difference in sex distribution was found between cases and controls. No difference was observed with regard to smoking (Table 1) (7,31).…”

Section: Resultsmentioning

confidence: 89%

“…The difference in cumulative asbestos exposure between the cases and controls was statistically significant (t=4.78, p=0.000) (7,31).…”

Section: Resultsmentioning

confidence: 94%

“…Recent studies indicate that genetic polymorphisms play an important role in susceptibility to the development of asbestosis (7,(9)(10)(30)(31). To our knowledge, the association between asbestosis and CAT -262 C>T polymorphism has not been studied so far.…”

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confidence: 90%

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Asbestosis and Catalase Genetic Polymorphism

Franko

Dolžan

Arnerić

et al. 2008

Archives of Industrial Hygiene and Toxicology

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Catalase (CAT) is part of the enzymatic defense system against reactive oxygen species (ROS), known to be involved in the pathogenesis of asbestosis. This study investigates whether CAT -262 C>T genetic polymorphism influences the risk of asbestosis in workers occupationally exposed to asbestos. The nested case-control study included 262 cases with asbestosis and 265 controls with no asbestosrelated disease. Data on cumulative asbestos exposure and smoking were available. A real-time PCR assay was introduced for genotyping CAT -262 C>T promoter polymorphism. A slightly elevated risk of asbestosis was observed in subjects with the CAT -262 TT genotype compared to others (OR=1.36, CI 0.70-2.62). This risk did not change substantially after adjustment by sex, age, and smoking, but the involvement of cumulative asbestos exposure changed the OR to 1.91 ). These findings indicate that the CAT -262 TT genotype may be slightly associated with an increased risk of asbestosis. No synergistic effect was found between cumulative asbestos exposure and the CAT -262 TT genotype, but cumulative asbestos exposure acted as a confounder. These results are an important contribution to understanding the interactions between genetic and environmental factors that may modify the risk of asbestosis.

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Section: Discussionsupporting

confidence: 81%

“…No significant difference in sex distribution was found between cases and controls. No difference was observed with regard to smoking (Table 1) (7,31).…”

Section: Resultsmentioning

confidence: 89%

“…The difference in cumulative asbestos exposure between the cases and controls was statistically significant (t=4.78, p=0.000) (7,31).…”

Section: Resultsmentioning

confidence: 94%

mentioning

confidence: 90%

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Asbestosis and Catalase Genetic Polymorphism

Franko

Dolžan

Arnerić

et al. 2008

Archives of Industrial Hygiene and Toxicology

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“…Conversely, the GSTT1 null genotype has been suggested as a protective factor against the development of asbestosis [9]. In addition to GSTM1 and GSTT1, the GSTP1 genotype has been associated with asbestos-related pulmonary fibrosis [10].…”

mentioning

confidence: 99%

Genetic susceptibility to asbestos-related fibrotic pleuropulmonary changes

Kukkonen

Hämäläinen²,

Kaleva

et al. 2010

European Respiratory Journal

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The objective of this study was to determine whether genetic polymorphisms in enzymes that metabolise oxidative agents modify the individual susceptibility to developing asbestos and smoking-related pleuropulmonary changes.Nine polymorphisms of six genes (EPHX1, GSTM1, GSTM3, GSTP1, GSTT1 and NAT2) were genotyped from 1,008 Finnish asbestos-exposed workers. The genotype data were compared to signs of lung fibrosis and pleural thickenings, as well as with total lung capacity, single-breath diffusing capacity of the lung for carbon monoxide (DL,CO) and specific diffusing capacity (expressed as DL,CO per unit of alveolar volume (VA)).The GSTT1 deletion polymorphism was associated with fibrotic changes (p50.003), and decreased DL,CO (p50.02) and DL,CO/VA (p50.002), and the GSTM1 deletion polymorphism was associated with the greatest thickness of pleural plaques (p50.009). On further analysis, the GSTT1 null genotype was found to pose over a three-fold risk for severe fibrotic changes (OR 3.12, 95% CI 1.51-6.43), and around two-fold risks for decreased DL,CO (OR 1.77, 95% CI 1.06-2.95) and DL,CO/VA (OR 2.37, 95% CI 1.33-4.23). In addition, the GSTM1 null genotype showed an elevated risk (OR 1.36, 95% CI 1.03-1.80) for thicker pleural plaques.Our data suggest that inherited detoxification capacity may affect the development and severity of asbestos and smoking-related nonmalignant pulmonary changes.

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