DNA damage to cochlear hair cells caused by 8-oxoguanine (8-oxoG) is essential for the development of noise-induced hearing loss (NIHL). Human 8-oxoG DNA glycosylase1 (hOGG1) is a key enzyme in the base excision repair (BER) pathway that eliminates 8-oxoG. Many epidemiological and functional studies have suggested that the hOGG1 Ser326Cys polymorphism (rs1052133) is associated with many diseases. The purpose of this investigation was to investigate whether the hOGG1 Ser326Cys polymorphism in the human BER pathway is associated with genetic susceptibility to NIHL in a Chinese population. This polymorphism was genotyped among 612 workers with NIHL and 615 workers with normal hearing. We found that individuals with the hOGG1 Cys/Cys genotype had a statistically significantly increased risk of NIHL compared with those who carried the hOGG1 Ser/Ser genotype (adjusted OR = 1.59, 95% CI = 1.13–2.25) and this increased risk was more pronounced among the workers in the 15- to 25- and >25-year noise exposure time, 85–92 dB(A) noise exposure level, ever smoking, and ever drinking groups, similar effects were also observed in a recessive model. In summary, our data suggested that the hOGG1 Cys/Cys genotype may be a genetic susceptibility marker for NIHL in the Chinese Han population.

Coffee consumption has been linked to risk of colorectal cancer theoretically, but the findings were conflicting from observational studies. Results from the recent meta-analysis suggested a moderate favorable effect of coffee consumption on colorectal cancer risk, especially for colon cancer. However, the relationship, if exists, between coffee consumption and colorectal cancer risk is unclear. Thus, the dose-response relationship was assessed by restricted cubic spline model and multivariate random-effect meta-regression. The results suggested that a significant association was found between coffee consumption and decreased risk of colorectal and colon cancer among subjects consuming ≥4 cups of coffee per day. A potential nonlinear relationship should be assessed before assuming a linear relationship.

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A meta-analysis was conducted to assess the effect of glutathione peroxidase1 (GPX1) gene Pro200Leu (rs1050450) polymorphism on cancer risk. A comprehensive search was performed to identify all studies on the association of GPX1 gene Pro200Leu polymorphism with cancer risk. The fixed or random effect pooled measure was selected based on homogeneity test among studies. Heterogeneity among studies was evaluated using the I (2). Potential sources of between-study heterogeneity were explored by meta-regression and the sensitivity analysis. Publication bias was estimated using Egger's linear regression test. 35 published articles with 36 results were identified involving 16,920 cases and 19,946 controls. Results from the articles that both obeyed Hardy-Weinberg equilibrium in controls and met high quality design, showed no significant association of GPX1 gene Pro200Leu polymorphism with cancer risk in any of dominant (OR = 1.05, 95 %CI = 0.98-1.12), recessive (OR = 1.04 (0.95-1.13), and TT versus CC (OR = 1.05, 95 %CI = 0.97-1.15) models, and the findings were consistent considering the stratified analysis by cancer type. However, multivariate-adjusted ORs from articles that both obeyed Hardy-Weinberg equilibrium in controls and met high quality design, showed a significant association considering dominant (OR = 1.22, 95 %CI = 1.06-1.41), TT versus CC (OR = 1.16, 95 %CI = 1.02-1.32) models, and a marginally significant association was found considering TC versus CC (OR = 1.11, 95 %CI = 0.99-1.25) model. And compared with the CC genotype, the erythrocyte GPX activity was significantly lower for TT genotype: the standardized mean difference (SMD) = -0.37, 95 %CI = (-0.624, -0.118), and CT genotype: SMD = -0.19, 95 %CI = (-0.37, -0.002). The association of GPX1 gene Pro200Leu polymorphism with cancer risk might be influenced by confounders.

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