Abstract
BackgroundChronic gastritis along with Helicobacter pylori (H. pylori) infection has been implicated in inflammatory response-related genes linked to the causation of gastric cancer. Glutathione S-transferase Pi (GSTP1) plays a role in regulating oxidative stress and detoxification against carcinogenesis. In this study, we aimed to determine whether an antioxidant-rich diet is associated with gastric cancer risk and identify how this association could be altered by GSTP1 genetic variants.MethodsThis study included 1,245 participants (415 cases and 830 controls) matched for age and sex. The dietary antioxidant capacity was estimated based on the oxygen radical absorbance capacity (ORAC) incorporated with a semiquantitative food frequency questionnaire. Five single nucleotide polymorphisms (SNPs) of GSTP1 (rs1695, rs749174, rs1871042, rs4891, and rs947895) were selected among the exome array genotype data.ResultsHigh dietary ORAC was inversely associated with gastric cancer (hydrophilic ORAC OR T3 vs . T1, 95% CI = 0.57, 0.39–0.82, P = 0.004; lipophilic ORAC = 0.66, 0.45–0.95, P = 0.021; total phenolics = 0.57, 0.39–0.83, P = 0.005). The polymorphism rs1871042 increased the risk of gastric cancer (OR, 95% CI = 1.55, 1.10–2.16, P = 0.01, CT+TT vs. CC). A remarkably reduced risk of gastric cancer was observed among those who had a high dietary ORAC according to rs1871042 polymorphism (hydrophilic ORAC OR T3 vs . T1, 95% CI = 0.36, 0.17–0.78, P for trend = 0.013; lipophilic ORAC = 0.58, 0.37–0.93, P for trend = 0.021; total phenolics = 0.38, 0.17–0.83, P for trend = 0.019).ConclusionsOur findings indicate that dietary ORAC intake may be inversely associated with the risk of gastric cancer altered by genetic variants of GSTP1, providing new intervention strategies for gastric cancer patients.
Highlights
Chronic gastritis along with Helicobacter pylori (H. pylori) infection has been implicated in inflammatory response-related genes linked to the causation of gastric cancer
Given that the risk of Gastric cancer (GC) is linked to dietary factors and the inflammatory response associated with H. pylori infection, this study focused on exploring the integrated and synergistic effects of antioxidants on GC using the oxygen radical absorbance capacity (ORAC) of a diet
ORAC, oxygen radical absorbance capacity; hydrophilic ORAC (H-ORAC), hydrophilic oxygen radical absorbance capacity; lipophilic ORAC (L-ORAC), lipophilic oxygen radical absorbance capacity; TPs, total phenolics; TE, trolox equivalents; GAE, gallic acid equivalents; T, tertile; odds ratios (OR), odds ratio; 95% confidence intervals (CI), 95% confidence interval
Summary
Chronic gastritis along with Helicobacter pylori (H. pylori) infection has been implicated in inflammatory response-related genes linked to the causation of gastric cancer. We aimed to determine whether an antioxidant-rich diet is associated with gastric cancer risk and identify how this association could be altered by GSTP1 genetic variants. There are several major risk factors for the development of GC, including Helicobacter pylori (H. pylori) infection, smoking, alcohol consumption, obesity, and excess sodium intake [2]. Helicobacter pylori infection is associated with an increased risk of non-cardia GC and cardia GC according to several studies targeting East Asian countries, such as Korea [5, 6]. Evidence suggests that gastritis derived from chronic inflammation of normal mucosa may be linked to various other dietary factors, such as a high intake of salted or preserved foods and grilled or processed meats and a low intake of fruits [7, 8]
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