Polymorphisms of glutathione S-transferase M1, T1, and P1 in patients with HBV-related liver cirrhosis, chronic hepatitis, and normal carriers

Role of Glutathione S Transferase M1 and T1 Gene Polymorphism in Hepatitis B Related Liver Diseases and Cryptogenic Cirrhosis

“…These studies have shown that GSTM1 null genotype was more prevalent in cryptogenic cirrhosis as well as hepatitis B cirrhosis. 14,15 Our results also show that GSTM1 null genotype was more prevalent in chronic hepatitis B, hepatitis B cirrhosis and cryptogenic cirrhosis as compared to control population, thereby confirming previous findings. However the GSTT1 null genotypes were not found to differ significantly between any of the groups.…”

“…14 Later a similar study was undertaken to find the correlation if any between polymorphisms in GSTM1, GSTT1, and GSTP1 in patients with HBV-related, chronic hepatitis, liver cirrhosis and normal carriers, they observed a higher frequency of the GSTM1 null genotype in patients with cirrhosis and chronic hepatitis compared to normal carriers. 15 The present study was undertaken to study the role of GSTM1 and T1 gene polymorphisms in different stages of HBV infection namely HBV inactive carrier, chronic hepatitis B and cirrhosis, and cryptogenic cirrhosis.…”

Accelerated liver fibrosis in hepatitis B virus transgenic mice: Involvement of natural killer T cells

“…Most studies on the relationship between HBV infection and liver fibrosis were based on clinical data, the results of which demonstrated that the pathologic mechanisms are relatively variable and complex. For example, the human gene polymorphisms such as glutathione and angiotensinogen were associated with HBV‐related liver cirrhosis11, 12 and the HBV gene mutation was another factor in the severity of the disease 13. Recently, one study revealed that the HBV x gene‐transfected hepatocyte cell lines could activate human HSCs, suggesting a direct interaction between HBV infection and activation of HSCs 14.…”

Glutathione S-transferase M1, T1, and P1 polymorphisms as susceptibility factors for noise-induced temporary threshold shift

“…In previous human studies, polymorphic deletions of GSTM1 and GSTT1 have been linked to the inactivation of antioxidant protection and the pathogenesis of several diseases in which oxidative stress had been implicated. The diseases included various forms of cancer (Strange et al, 2001;Agalliu et al, 2006;Hosgood et al, 2007;Singh et al, 2008), arsenic related skin lesion (McCarty et al, 2007), multiple sclerosis (Mann et al, 2000), rheumatoid arthritis (Yun et al, 2005), Parkinson's disease (Tan et al, 2000), liver cirrhosis (Ghobadloo et al, 2004;Mohammadzadeh Ghobadloo et al, 2006), asthma (Ivaschenko et al, 2002;Lee et al, 2004;Mak et al, 2007), and chronic obstructive pulmonary disease (Cheng et al, 2004;Zidzik et al, 2008). Based on previous studies of NIHL, noise-exposed workers with GSTM1 null genotype and those with GSTT1 null genotype are at high risk for hearing impairment (Rabinowitz et al, 2002;Yang et al, 2005).…”