Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulin resistance has been assigned a pivotal role in the pathological progression associated with type 2 diabetes and other chronic metabolic diseases. However, the molecular mechanism involved in this progression is still incompletely understood, and there are still no effective approaches to scavenge it. Many biological molecules, such as ROS, IRS-1, PI3K, have been identified involving in the causes of insulin resistance. Restoring these molecules could ameliorate the phenomenon of insulin resistance. BVR was known for a long time solely as an enzyme reducing biliverdin to bilirubin in the heme metabolic pathway. Presently, accumulative research data showed that BVR was a strong antioxidant enzyme, which could scavenge the excess ROS, and the characteristics of kinase activity and binding with p85 could modulate the biological function of IRS-1 and PI3K. We hypothesize that BVR has a significant role in the progression of insulin resistance, and it will be a promising therapeutic target for treating insulin resistance.
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PMID:Old biliverdin reductase: links to insulin resistance and may be a novel therapeutic target. 1839 54

This study investigated the possible interaction between the heme oxygenase (HO)/biliverdin reductase (BVR) and nitric oxide synthase (NOS) pathway in murine gastric fundus and jejunum, since previous studies have shown that both HO-2 and BVR are expressed in interstitial cells of Cajal (ICCs) and co-localized with neuronal NOS in a large proportion of myenteric neurons along the gastrointestinal tract. Neither HO inhibition by chromium mesoporphyrin (CrMP) nor co-incubation with CO or biliverdin/bilirubin affected nitrergic neurotransmission - i.e. relaxations induced by non-adrenergic non-cholinergic (NANC) nerve stimulation or exogenous NO - under normal physiological conditions. However, biliverdin/bilirubin reversed the inhibitory effect of the superoxide generator LY83583 on exogenous NO-induced relaxations in both tissues. When gastric fundus muscle strips were depleted of the endogenous antioxidant Cu/Zn superoxide dismutase (SOD) by the Cu-chelator DETCA, electrically induced NANC relaxations were also affected by LY82583; however, biliverdin/bilirubin could not substitute for the loss of Cu/Zn SOD when this specific antioxidant enzyme was depleted. In jejunal muscle strips, the combination DETCA plus LY83583 nearly abolished contractile phasic activity and, hence, did not allow studying nitrergic relaxation in these experimental conditions. In conclusion, this study does not establish a role for HO/CO in inhibitory NANC neurotransmission in murine gastric fundus and jejunum under normal physiological conditions. However, the antioxidants biliverdin/bilirubin might play an important role in the protection of the nitrergic neurotransmitter against oxidative stress.
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PMID:Investigation of a possible interaction between the heme oxygenase/biliverdin reductase and nitric oxide synthase pathway in murine gastric fundus and jejunum. 1860 39

This review will discuss some issues related to the risk/benefit profile of the use of dietary antioxidants. Thus, recent progress regarding the potential benefit of dietary antioxidants in the treatment of chronic diseases with a special focus on immune system and neurodegenerative disorders will be discussed here. It is well established that reactive oxygen species (ROS) play an important role in the etiology of numerous diseases, such as atherosclerosis, diabetes and cancer. Among the physiological defense system of the cell, the relevance of antioxidant molecules, such as glutathione and vitamins is quite well established. Recently, the interest of researchers has, for example, been conveyed on antioxidant enzyme systems, such as the heme oxygenase/biliverdin reductase system, which appears modulated by dietary antioxidant molecules, including polyphenols and beta-carotene. These systems possibly counteract oxidative damage very efficiently and finally modulate the activity of oxidative phenomena occurring, for instance, during pathophysiological processes. Although evidence shows that antioxidant treatment results in cytoprotection, the potential clinical benefit deriving from both nutritional and supplemental antioxidants is still under wide debate. In this line, the inappropriate assumption of some lipophylic vitamins has been associated with increased incidence of cancer rather than with beneficial effects.
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PMID:The role of antioxidant supplement in immune system, neoplastic, and neurodegenerative disorders: a point of view for an assessment of the risk/benefit profile. 1882 65

Biliverdin reductase A (BLVRA) is a powerful intracellular antioxidant enzyme and an antagonist to insulin-mediated glucose uptake by the cells. Increased oxidative stress and insulin-resistance (IR) are associated with increased risk for hypertension. Therefore, we hypothesized that BLVRA might be attributable to the variation of susceptibility to essential hypertension, and investigated single nucleotide polymorphism (SNP) rs699512 (Thr3Ala), the only common non-synonymous SNP within BLVRA, in population-based samples of 999 Kazak herdsmen from the villages in Xinjiang, China. The minor allele of SNP rs699512 reduced the risk of essential hypertension (age- and gender-adjusted odds ratio 0.76; 95% confidence interval 0.61-0.94; p = 0.010). Single nucleotide polymorphism rs699512 showed association with both systolic and diastolic blood pressures: the minor allele homozygous carriers had lowest systolic and diastolic blood pressures (139.6 mmHg, 89.6mmHg), followed by heterozygous carriers (145.3 mmHg, 92.3 mmHg), and then major allele homozygous carriers (150.3 mmHg, 95.1 mmHg) (p = 0.005 and 0.009, respectively). These findings provide the first genetic evidence for the role of BLVRA on the susceptibility to human essential hypertension and blood pressure.
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PMID:Association of a BLVRA common polymorphism with essential hypertension and blood pressure in Kazaks. 2172 74