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Exercise Redox Signalling
Published in James N. Cobley, Gareth W. Davison, Oxidative Eustress in Exercise Physiology, 2022
Ruy A. Louzada, Jessica Bouviere, Rodrigo S. Fortunato, Denise P. Carvalho
Finally, the importance of modulating the redox environment status was recently confirmed by the discovery of an endogenous factor capable of promoting “reductive stress” that counteract the physiological ROS bursts induced by exercise (Takamura, 2020). Elegantly, Musi et al. demonstrated that selenoprotein P (SEPP1) enables communication between the liver and muscle to upregulate GPX1, which maintains a reduced intracellular environment that is related to a lack of ROS-induced AMPK/PGC-1α activation following physical exercise. As a result, the beneficial effects of exercise are hampered in some obese patients with high circulating levels of SEPP1 (Misu et al., 2017).
British Journal of Biomedical Science in 2018: what have we learned?
Published in British Journal of Biomedical Science, 2019
Oxidative stress may be linked to the initiation and progression of breast cancer, and may be countered by selenoproteins, many of which have been shown to have redox functions, acting as antioxidants. Mohammaddoust et al. [21] probed the association of SNPs in SEPP1 and SEP15 with the risk of breast cancer in 150 cases and 200 cancer-free controls using PCR-RFLP and allele-specific PCR (AS-PCR). The AA genotype (Thr/Thr) for SEPP1 and AA genotype for SEP15 were linked to a higher risk of breast cancer (OR = 3.89; 95% CI, 2.02–7.49; P < 0.0001 and OR = 2.82; 95% CI, 1.04–7.62; p = 0.04, respectively). In addition, the SEPP1 A allele was linked with higher breast cancer risk, pointing to the possible use of these SNPs in routine screening. Mashayekhi et al. [22] also investigated breast cancer, looking at miR-27a, mir-196a2 and miR-146a in 353 cases and 353 controls. The principle finding was that the CC genotype of miR-146a (rs2910164) was seen in 45 (12.7%) patients with breast cancer and 18 (5.1%) controls (OR 4.09 [95% CI 2.19–7.67] P < 0.001) whilst the minor allele G of miR-27a was associated with a decreased risk of breast cancer (OR 0.24 [95% CI 0.14–0.42] P < 0.001) suggesting that these variants contribute to breast cancer and so may also, one day, be used in a routine setting.
The relationship between gestational diabetes mellitus and selenoprotein-P plasma 1 (SEPP1) gene polymorphisms
Published in Gynecological Endocrinology, 2018
Gulhan Akbaba, Eren Akbaba, Cem Sahin, Murat Kara
Selenoprotein P is encoded by SEPP1 gene. Genetic variations in SEPP1 were found to be associated with certain metabolic phenotypes. Specifically, rs146125471 and rs28919926 polymorphisms were associated to acute insulin response and rs16872762 polymorphism was associated to fasting insulin level. In a meta-analysis including three different ethnic groups, on the other hand, rs13154178 polymorphism was correlated with fasting glucose level [18].
SEPP1 and SEP15 gene polymorphisms and susceptibility to breast cancer
Published in British Journal of Biomedical Science, 2018
Samaneh Mohammaddoust, Zivar Salehi, Hamid Saeidi Saedi
Breast cancer is the most commonly diagnosed type of cancer among women worldwide, (second most common cancer overall) [1]. Cancer onset and progression have been linked to oxidative stress by increasing DNA mutations or inducing DNA damage, genome instability and cell proliferation, and therefore antioxidant agent could interfere with carcinogenesis [2]. Single nucleotide polymorphisms may have functional effects on gene expression and protein activity [3]. Selenoprotein P (Sepp1) is the most abundant selenoprotein in serum and delivers selenium to tissues, carrying ten selenocysteine (Sec) residues per polypeptide. Sepp1 has been postulated as a defence mechanism to defend against oxidative injury in the extracellular space [4]. The best-studied polymorphism of this selenoprotein includes Ala234Thr (rs3877899) that is associated with a G/A transition at position 24731 of mRNA, with the amino acid change from alanine to threonine in the codon 234. The major allele G favours the production of a Se-rich 60 kDa isoform, while allele A favours the 50 kDa low Se isoform. This polymorphism affects selenium’s bioavailability for the synthesis of all other selenoproteins by influencing the body’s selenium status, effectiveness of supplementation, and selenium supply to target tissues [5]. SEP15 is localized on chromosome 1p31, a locus often deleted or mutated in human cancers. The gene product, 15 kDa selenoprotein (Sep15), exhibits redox activity and may have antioxidant properties [6]. G1125A (rs5859) is a single nucleotide polymorphism within the SEP15 SECIS element (3′UTR), and is associated with G/A transition at position 1125. SNPs in the gene regions corresponding to 3′UTR could potentially influence expression because of the key role of the SECIS and 3′UTR–protein interactions in Sec incorporation [7]. SEPP1 (rs3877899) and SEP15 (rs5859) are two important polymorphisms that several studies have linked with various cancers, including risk of breast cancer, lung cancer in smokers, rectal cancer risk, and risk of prostate cancer. Data from these association studies have shown that the investigated SNPs altered the expression or function of selenoproteins and may increase the risk of developing cancer. We hypothesized that the Sepp1 and Sep15 polymorphisms are linked to breast cancer.