Effect of Selenium on Connexin Expression, Angiogenesis, and Antioxidant Status in Diabetic Wound Healing

Bajpai, Surabhi; Mishra, Manish; Kumar, Hemant; Tripathi, Kamlakar; Singh, Santosh Kumar; Pandey, Harsh; Singh, Rakesh Kumar

doi:10.1007/s12011-011-9097-7

Cited by 35 publications

(22 citation statements)

References 32 publications

(34 reference statements)

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“…Pretreatment with Se, Zn and the combination, but not Cr(pic)3 significantly increased the cardiac levels of VEGF, which implies that these elements had angiogenic effects in hypoxic conditions. While Se exhibited angiogenic effects in our study and in diabetic states (65), previous data support an anti-angiogenic effect of Se in the chemoprevention of many types of cancer (66,67) which imply that Se may act as anti-angiogenic or angiogenic depending on physiologic and metabolic conditions.…”

supporting

confidence: 70%

Preventive Effects of Selenium Yeast, Chromium Picolinate, Zinc Sulfate and their Combination on Oxidative Stress, Inflammation, Impaired Angiogenesis and Atherogenesis in Myocardial Infarction in Rats

et al. 2014

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Purpose: Accumulating evidences suggest a critical role of trace metal dyshemostasis in oxidative stress and cardiac dysfunction after myocardial infarction (MI). This study investigated the cardioprotective effects of selenium yeast (Se), chromium picolinate Cr(pic)3, zinc sulfate (Zn) and their combination on isoproterenol (ISO)-induced MI. Methods: Rats were divided into six groups: normal control, ISO control, Se-pretreated (0.1 mg/kg), Cr(pic)3-pretreated (400 µg/kg), Zn-pretreated (30 mg/kg) and metal combination-pretreated groups. All metals were administered for 28 days and at the 27th day, MI was induced by subcutaneous injection of ISO (85 mg/kg) once for two consecutive days. Results: ISO control group showed hyperlipidemia, elevation of cardiac biomarkers and lipid peroxidation and increased immunostaining of p47 phox NADPH oxidase subunit in addition to decreased levels of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). Cardiac levels of tumor necrosis factor-α (TNF-α) were increased, while vascular endothelial growth factor (VEGF, the major angiogenic factor) was decreased. Pretreatment with Se normalized the cardiac enzymes, lipid peroxidation, GSH, SOD, CAT, GPx, TNF-α and VEGF (P<0.001) and reduced the immunostaining of p47 phox subunit. However, Se failed to correct the dyslipidemia. Cr(pic)3 significantly improved lipid profile (P<0.001) and all other biochemical deviations except for VEGF. Zn, but to lesser extent, reduced the oxidative damage and TNF-α levels and improved both dyslipidemia and angiogenesis. Combination therapy exhibited less prominent protection compared to individual metals. Conclusion: Daily supplementation with trace metals is promising for improving myocardial performance via preventing oxidative damage, induction of angiogenesis, anti-inflammatory and/or anti-hyperlipidemic mechanisms.This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

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confidence: 70%

Preventive Effects of Selenium Yeast, Chromium Picolinate, Zinc Sulfate and their Combination on Oxidative Stress, Inflammation, Impaired Angiogenesis and Atherogenesis in Myocardial Infarction in Rats

et al. 2014

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“…Tumors need specialized environments to grow and thrive in. As the tumor grows, new blood vessels need to form to provide the cells with oxygen and all of the treatment options selected are able to inhibit angiogenesis, except vitamin B and selenium, both of which show mixed results [408] , [409] , [410] , [411] , [412] , [413] , [414] , [415] , [416] , [417] , [418] , [419] . Interestingly though, in regards to other factors that contribute to the tumor microenvironment, all compounds are able to provide therapeutic value [395] , [420] , [421] , [422] , [423] , [424] .…”

Section: Complementary Effects On the Enabling Characteristics Of Canmentioning

confidence: 99%

Genomic instability in human cancer: Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition

Ferguson

Chen

Collins

et al. 2015

Seminars in Cancer Biology

259

215

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Genomic instability can initiate cancer, augment progression, and influence the overall prognosis of the affected patient. Genomic instability arises from many different pathways, such as telomere damage, centrosome amplification, epigenetic modifications, and DNA damage from endogenous and exogenous sources, and can be perpetuating, or limiting, through the induction of mutations or aneuploidy, both enabling and catastrophic. Many cancer treatments induce DNA damage to impair cell division on a global scale but it is accepted that personalized treatments, those that are tailored to the particular patient and type of cancer, must also be developed. In this review, we detail the mechanisms from which genomic instability arises and can lead to cancer, as well as treatments and measures that prevent genomic instability or take advantage of the cellular defects caused by genomic instability. In particular, we identify and discuss five priority targets against genomic instability: (1) prevention of DNA damage; (2) enhancement of DNA repair; (3) targeting deficient DNA repair; (4) impairing centrosome clustering; and, (5) inhibition of telomerase activity. Moreover, we highlight vitamin D and B, selenium, carotenoids, PARP inhibitors, resveratrol, and isothiocyanates as priority approaches against genomic instability. The prioritized target sites and approaches were cross validated to identify potential synergistic effects on a number of important areas of cancer biology.

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“…A transcriptomic analysis in normal rats showed that angiogenic genes were affected by selenite supplementation [64]. However, in diabetic mice, selenium (provided as selenite) has been shown to promote angiogenesis and, thereby, wound healing [65]. Both pro- and anti-apoptotic effects have been demonstrated with selenium supplementation.…”

Section: Biphasic Effects Of Selenium Statusmentioning

confidence: 99%

Selenistasis: Epistatic Effects of Selenium on Cardiovascular Phenotype

Joseph

Loscalzo

2013

Nutrients

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Although selenium metabolism is intricately linked to cardiovascular biology and function, and deficiency of selenium is associated with cardiac pathology, utilization of selenium in the prevention and treatment of cardiovascular disease remains an elusive goal. From a reductionist standpoint, the major function of selenium in vivo is antioxidant defense via its incorporation as selenocysteine into enzyme families such as glutathione peroxidases and thioredoxin reductases. In addition, selenium compounds are heterogeneous and have complex metabolic fates resulting in effects that are not entirely dependent on selenoprotein expression. This complex biology of selenium in vivo may underlie the fact that beneficial effects of selenium supplementation demonstrated in preclinical studies using models of oxidant stress-induced cardiovascular dysfunction, such as ischemia-reperfusion injury and myocardial infarction, have not been consistently observed in clinical trials. In fact, recent studies have yielded data that suggest that unselective supplementation of selenium may, indeed, be harmful. Interesting biologic actions of selenium are its simultaneous effects on redox balance and methylation status, a combination that may influence gene expression. These combined actions may explain some of the biphasic effects seen with low and high doses of selenium, the potentially harmful effects seen in normal individuals, and the beneficial effects noted in preclinical studies of disease. Given the complexity of selenium biology, systems biology approaches may be necessary to reach the goal of optimization of selenium status to promote health and prevent disease.

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Effect of Selenium on Connexin Expression, Angiogenesis, and Antioxidant Status in Diabetic Wound Healing

Cited by 35 publications

References 32 publications

Preventive Effects of Selenium Yeast, Chromium Picolinate, Zinc Sulfate and their Combination on Oxidative Stress, Inflammation, Impaired Angiogenesis and Atherogenesis in Myocardial Infarction in Rats

Preventive Effects of Selenium Yeast, Chromium Picolinate, Zinc Sulfate and their Combination on Oxidative Stress, Inflammation, Impaired Angiogenesis and Atherogenesis in Myocardial Infarction in Rats

Genomic instability in human cancer: Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition

Selenistasis: Epistatic Effects of Selenium on Cardiovascular Phenotype

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