GPX1 gene Pro200Leu polymorphism, erythrocyte GPX activity, and cancer risk

Hong, Zhi-Qiang; Tian, Changwei; Zhang, Xingliang

doi:10.1007/s11033-012-2234-3

Cited by 19 publications

(18 citation statements)

References 47 publications

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“…Increased understanding of the mechanisms that cells use to respond to mitochondrial oxidative stress in vivo is less thoroughly investigated to date and may be relevant in understanding the pathogenesis of complex disease, particularly as a reduced capacity to mount and antioxidant response is linked with a number of disease states [55, 56, 58, 59], as well as the ageing process [84]. …”

Section: Mitochondrial Stress Signalsmentioning

confidence: 99%

Mitochondrial Stress Signaling Promotes Cellular Adaptations

Barbour

Turner

2014

International Journal of Cell Biology

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Mitochondrial dysfunction has been implicated in the aetiology of many complex diseases, as well as the ageing process. Much of the research on mitochondrial dysfunction has focused on how mitochondrial damage may potentiate pathological phenotypes. The purpose of this review is to draw attention to the less well-studied mechanisms by which the cell adapts to mitochondrial perturbations. This involves communication of stress to the cell and successful induction of quality control responses, which include mitophagy, unfolded protein response, upregulation of antioxidant and DNA repair enzymes, morphological changes, and if all else fails apoptosis. The mitochondrion is an inherently stressful environment and we speculate that dysregulation of stress signaling or an inability to switch on these adaptations during times of mitochondrial stress may underpin mitochondrial dysfunction and hence amount to pathological states over time.

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Section: Mitochondrial Stress Signalsmentioning

confidence: 99%

Mitochondrial Stress Signaling Promotes Cellular Adaptations

Barbour

Turner

2014

International Journal of Cell Biology

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“…The results of a meta‐analysis performed by Men et al showed the significant correlation of the rs1050450 polymorphism with an increased risk of bladder cancer, while there was no significant association for prostate cancer . In addition, the meta‐analysis by Chen et al indicated the correlation of the individuals with variant Leu allele of rs1050450 with an increased cancer risk in dominant genetic model; however, Hong et al's meta‐analysis results showed no association of GPX1 gene rs1050450 polymorphism with cancer risk in any of dominant and recessive models . Recent study by Yang et al showed the effect of rs1050450 on breast cancer risk, while Nikic et al and Zhang et al showed no significant association between rs1050450 polymorphism and metastatic urothelial bladder and Gastric cancers, respectively.…”

Section: Discussionmentioning

confidence: 99%

The effects of the genetic polymorphisms of antioxidant enzymes on susceptibility to papillary thyroid carcinoma

et al. 2020

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Several lines of evidences have indicated that inflammation play an important role in the carcinogenesis. During the inflammatory processes, free radical species are produced from oxidative stress. In normal conditions, enzymatic and nonenzymatic antioxidants remove these products. Manganese superoxide dismutase (MnSOD), glutathione peroxidase‐1 (GPx‐1), and catalase (CAT) are three important enzymes. Therefore, this study aimed to evaluate the effects of MnSOD (SOD2), GPX‐1, and CAT genetic polymorphisms on papillary thyroid carcinoma (PTC) susceptibility. A total of 134 patients with PTC and 151 healthy controls were recruited to participate in this study. All samples were genotyped for SOD2 rs4880, GPX1 1050450, and CAT rs7943316 polymorphisms by polymerase chain reaction‐restriction fragment length polymorphism method. The frequencies of the rs1050450, rs4880, and rs7943316 alleles and genotypes were not different between PTC patients and controls. However, the TC genotype of SOD2 rs4880 polymorphism was significantly higher in males compared to that in females in PTC patients (odds ratio [OR], 3.9 [95% CI, 1.5–11], p = .007). The rs4880 polymorphism was also associated with higher stages (III‐IV) of PTC in dominant model. No significant correlation was found between GPX1‐rs1050450 and CAT‐rs7943316 polymorphisms and demographic, clinical, and pathological features of the disease. The SOD2 rs4880CT genotype was more frequent in males with PTC and patients with higher stages (III–IV) of disease (OR, 2.9 [95% CI, 1.1–7.7], p = .04). However, no significant association was found between GPX1‐rs1050450 and CAT‐rs7943316 variants and PTC or its demographic, clinical, and pathological features.

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“…GPX1 is cytosolic and produced in all tissues. The SNP rs1050450 (or GPX1 Pro198Leu) has been studied extensively in human disease and has already been linked to cancer risk [33], and oxidative stress related diseases [34]. The Leu198 variant results in a 10% reduced enzyme activity compared with the Pro198 variant [35], interfering with the overall capacity to respond to oxidative damage [34].…”

Section: Discussionmentioning

confidence: 99%

Association between Polymorphisms in Antioxidant Genes and Inflammatory Bowel Disease

et al. 2017

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Inflammation is the driving force in inflammatory bowel disease (IBD) and its link to oxidative stress and carcinogenesis has long been accepted. The antioxidant system of the intestinal mucosa in IBD is compromised resulting in increased oxidative injury. This defective antioxidant system may be the result of genetic variants in antioxidant genes, which can represent susceptibility factors for IBD, namely Crohn’s disease (CD) and ulcerative colitis (UC). Single nucleotide polymorphisms (SNPs) in the antioxidant genes SOD2 (rs4880) and GPX1 (rs1050450) were genotyped in a Portuguese population comprising 436 Crohn’s disease and 367 ulcerative colitis patients, and 434 healthy controls. We found that the AA genotype in GPX1 is associated with ulcerative colitis (OR = 1.93, adjusted P-value = 0.037). Moreover, we found nominal significant associations between SOD2 and Crohn’s disease susceptibility and disease subphenotypes but these did not withstand the correction for multiple testing. These findings indicate a possible link between disease phenotypes and antioxidant genes. These results suggest a potential role for antioxidant genes in IBD pathogenesis and should be considered in future association studies.

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GPX1 gene Pro200Leu polymorphism, erythrocyte GPX activity, and cancer risk

Cited by 19 publications

References 47 publications

Mitochondrial Stress Signaling Promotes Cellular Adaptations

Mitochondrial Stress Signaling Promotes Cellular Adaptations

The effects of the genetic polymorphisms of antioxidant enzymes on susceptibility to papillary thyroid carcinoma

Association between Polymorphisms in Antioxidant Genes and Inflammatory Bowel Disease

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