Abstract
Little is known about the contribution of each of the three superoxide dismutase isozymes (SODs) to the total SOD activity in extracellular fluids. This study was aimed to investigate the alterations in concentration/activity of (SODs) in plasma, in context of sex, obesity, exposition to cigarette smoke, and genotypic variability of five selected single nucleotide polymorphisms (SNPs) in genes SOD1, SOD2, SOD3. Men showed higher SOD1 concentration, lower SOD3 concentration and higher total antioxidative capacity (TAC) values. Intersexual variability was observed in concentration of copper, zinc, and cadmium. The obese showed higher total oxidative capacity regardless of sex. An increase in SOD2 activity was coexistent with obesity in men, and exposition to cigarette smoke in non-obese individuals. Additionally, in state of this exposition, Cu,Zn-SOD contribution to the total SOD was lower. Interestingly, over 90% of the obese were of C/T genotype of rs4880 (SOD2). Non-obese of T/T genotype (rs4880) were of lower total SOD activity due to decrease in both Cu,Zn-SOD and Mn-SOD activities. SNP rs2234694 was associated with differences in concentration of SODs, depending on obesity status. Correlations indicate that both TAC and SODs, together, may adapt to insulin resistance and inflammation-derived oxidative stress found in obesity. This topic should be further investigated.
Highlights
The demand to thoroughly understand the risk factors for developing obesity stems from the worldwide increase in prevalence of this disease [1], especially in the recent years
This study focuses on superoxide dismutases (SODs), a vital family of enzymatic antioxidants, which neutralize superoxide anion
No significant differences between women and men were found in values of SOD activity, men were characterized of significantly higher SOD1 concentration (p < 0.00001) and lower SOD3 concentration (p ≈ 0.0214 and p ≈ 0.0643 for SOD3 and SOD3, respectively) in plasma
Summary
The demand to thoroughly understand the risk factors for developing obesity stems from the worldwide increase in prevalence of this disease [1], especially in the recent years. It is commonly claimed that oxidative stress, coexisting with dyslipidemia, aberrant immunological response, disorders of the electrolyte balance, mitochondrial dysfunction, increased secretion of proinflammatory adipokines [2,3,4,5], and activation of inflammasomes and toll-like receptors contribute to the state of meta-inflammation, disorders such as insulin resistance, type 2 diabetes, and atherosclerosis often co-existent with obesity [6]. Excessive ROS generation and deficiency in antioxidative capacity caused by inactivation of enzymatic antioxidants, partly in the process of enzyme glycation, lead to disorders in lipid and carbohydrate metabolism and oxidative damage in proteins and DNA [10,11]. Activation of protein kinase C by diacylglycerol and advanced glycation end products formed from glyceraldehyde 3-phosphate (in the state of GAPDH activity deficiency) causes phosphorylation (inactivation) of insulin receptor substrate-1 (IRS-1), leading to insulin resistance [15,16,17]. The state of insulin resistance in obesity is promoted by disorders in modulation of the processes of secretion and degradation of insulin (due to hypozincemia) [18,19], glycation of insulin [20], “leptin resistance” causing accumulation of triglycerides in muscle tissue [21,22,23] and disorders in secretion of neuropeptides [24]
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