A higher catalytic efficiency than GSTP1 Ile/Val or Val/Val for most environmental carcinogens, including cytokines produced by H. pylori infection. These cytokines that could not be detoxified by GSTP1 could directly induce gastric mucosal damage and eventually lead to development of atrophic gastritis and even gastric cancer. The exact molecular biology mechanisms need further exploration. Tobacco smoking and alcohol consumption are the main known etiological factors of some cancers. In this study, we observed that higher ratios of people in the gastric cancer group had consumed tobacco and alcohol, compared with the controls. This finding indicated that alcohol and tobacco consumption are highly associated with increased risk for gastric cancer. Long-term tobacco smoking and alcohol consumption have been shown to contribute to carcinogenesis. Tobacco consumption can significantly increase nuclear hypoxia-inducible factor -1a expression, and alcohol can increase protein levels of c-fos and cjun proto-oncogenes. Association of the GSTP1 Val/Val genotype with smoking or alcohol consumption could significantly increase atrophic gastritis and gastric cancer risk. This phenomenon might be caused by alterations in catalytic efficiency between tobacco and alcohol constituents and the polymorphic GSTP1 gene. These findings provide a possible molecular explanation for the synergistic effect of smoking and alcohol consumption on gastric cancer development. However, details of the mechanism must be verified by other well-designed experiments. In conclusion, our results suggest that polymorphism of GSTP1 may contribute to gastric cancer susceptibility in the Chinese population. Moreover, the combined effect of GSTP1 Val allele with environmental carcinogens significantly increases the risk of gastric cancer development. Herbivory and neighboring plant competition for resources are two of the most important biotic forces affecting plant distributions and fitness. Competition, resource availability, and herbivory can affect levels of defensive compounds in plants, since chemical defense is a plastic response. Production of secondary metabolites is often associated with reduced fitness in terms of lower growth and reproduction. This trade-off between investment in plant defense versus growth and reproduction is termed an allocation cost. However, comparisons between defense and growth or reproduction may be insufficient to quantify the costs of defense because natural selection may strongly favor reductions in trade-offs between such important activities as growth, reproduction, and defense. Physiological parameters can be more useful than growth rates for quantifying the cost of plant defenses. Physiological costs, such as reductions in photosynthetic enzymes or the biosynthesis of other proteins required for primary metabolism are said to arise from ‘metabolic competition’ between defense production and primary metabolic functions. Further examination of physiological costs is important for determining the mechanisms underlying allocation costs and for understanding interactions between pathways leading to primary and secondary metabolites. In addition, despite the notable contributions of induced defense literature to understanding costs of chemical defense, it may be particularly interesting to study costs in constitutive LY2109761 700874-71-1 defenses to understand the baseline value plants place on tissue retention. In terms of physiological costs.