Evidence suggests an association between obesity and oxidative stress caused by superoxide production. Since the dismutation of superoxide is catalyzed by superoxide dismutase enzymes, we tested the association between obesity and Ala16Val manganese-dependent superoxide dismutase gene (MnSOD) polymorphism. We analyzed 815 free-living community subjects (> or =60 years old) grouped into subjects who were either obese (BMI > or = 30 kg/m(2)) or non-obese (BMI < 25 kg/m(2)). Additionally, we investigated the possible interaction between the Ala16Val MnSOD gene polymorphism and obesity in the modulation of biochemical and nutritional variables. We found a positive association between MnSOD polymorphism and obesity, since higher VV frequency (28.2%) was observed in the obese group (P = 0.002, odds ratio 1.949, 95% CI: 1.223-3.008). This result was independent of sex, age, diabetes, dyslipidemia, hypertension, and metabolic syndrome. A possible biological explanation of the association described here could be a chronic state of superoxide enzyme imbalance present in VV carriers, which could affect differential metabolic pathways contributing to the obese state.

Obesity is considered a chronic low-grade inflammatory state associated with a chronic oxidative stress caused by superoxide production (O(2)(-)). The superoxide dismutase manganese dependent (SOD2) catalyzes O(2)(-) in H(2)O(2) into mitochondria and is encoded by a single gene that presents a common polymorphism that results in the replacement of alanine (A) with a valine (V) in the 16 codon. This polymorphism has been implicated in a decreased efficiency of SOD2 transport into targeted mitochondria in V allele carriers. Previous studies described an association between VV genotype and metabolic diseases, including obesity and diabetes. However, the causal mechanisms to explain this association need to be more elucidated. We postulated that the polymorphism could influence the inflammatory response. To test our hypothesis, we evaluated the in vitro cytokines production by human peripheral blood mononuclear cells (PBMCs) carrier's different Ala16Val-SOD2 genotypes (IL-1, IL-6, IL-10, TNF-α, IFN-γ). Additionally, we evaluated if the culture medium glucose, enriched insulin, could influence the cytokine production. Higher levels of proinflammatory cytokines were observed in VV-PBMCs when compared to AA-PBMCs. However, the culture medium glucose and enriched insulin did not affect cytokine production. The results suggest that Ala16Val-SOD2 gene polymorphism could trigger the PBMCs proinflammatory cytokines level. However, discerning if a similar mechanism occurs in fat cells is an open question.

This study aimed to assess the potential protective effect of organic purple grape juice (PGJ) on oxidative stress produced by an exhaustive exercise bout in rats. To test this hypothesis, rats were acutely treated with organic PGJ (Vitis labrusca) and subsequently submitted to an exhaustive exercise bout. Parameters of oxidative stress, such as thiobarbituric acid reactive species (TBARS) levels, 2',7',-dichlorofluorescein diacetate (DCFH-DA) oxidation, and nonprotein sulfhydryl levels (NP-SH) in the brain, skeletal muscle, and blood, were evaluated. Enzyme activity of Na(+),K(+)-ATPase, Ca(2+)-ATPase, and δ-aminolevulinate dehydratase (δ-ALA-D) in the brain, skeletal muscle, and blood were also assayed. Statistical analysis showed that the exhaustive exercise bout increased TBARS levels and DCFH-DA oxidation, and decreased NP-SH levels in rat tissue. Ca(2+)-ATPase activity was increased in groups exposed to both exercise and PGJ treatment. The results indicate that organic PGJ intake was able to protect against the oxidative damage caused by an exhaustive exercise bout in different rat tissues.

These data reflect the importance of hormones and growth factors in the early stages of life, when the mammary gland is in development and therefore more vulnerable to proliferative stimuli.

Several epidemiological studies have investigated the association between the dietary flavonoid intake and gastric cancer (GC) risk; however, the results remain inconclusive. Investigating the relationship between the different classes of flavonoids and the histological types and origin of GC can be of interest to the research community. We used data from a population-based multi-case control study (MCC-Spain) obtained from 12 different regions of Spain. 2700 controls and 329 GC cases were included in this study. Odds ratios (ORs) were calculated using the mixed effects logistic regression considering quartiles of flavonoid intakes and log2. Flavonoid intake was associated with a lower GC risk (ORlog2 = 0.76; 95% CI = 0.65–0.89; ORq4vsq1 = 0.60; 95%CI = 0.40–0.89; ptrend = 0.007). Inverse and statistically significant associations were observed with anthocyanidins, chalcones, dihydroflavonols and flavan-3-ols. The isoflavanoid intake was positively associated with higher cancer risk, but without reaching a statistical significance. In general, no differences were observed in the GC risk according to the location and histological type. The flavonoid intake seems to be a protective factor against GC within the MCC-study. This effect may vary depending on the flavonoid class but not by the histological type and location of the tumor. Broader studies with larger sample size and greater geographical variability are necessary.