Caloric restriction improves the redox homeostasis in the aging male rat heart even when started in middle-adulthood and when the body weight is stable.

Evidence indicates that maintenance of redox homeostasis is fundamental for cellular longevity. Caloric-restriction (CR) is said to decrease the formation of oxidatively modified cellular macromolecules and improve health. On the other hand, some studies indicate that many CR studies are flawed, because ad libitum fed rats are not well-controlled. Thus, it is claimed that purported beneficial effects of CR could be not due to real CR effect, but due to control animals going obese. Also, it remains to be elucidated whether effects of CR could be observed even when CR is started in mid-adulthood. Male Sprague-Dawley rats were grouped as: non-CR 6-month-old rats (n = 7), 24-month-old rats subjected to 40% CR for 6 months between 18th and 24th months (n = 8), and non-CR 24-month-old animals (n = 8). We investigated 16 previously validated biomarkers of macromolecular redox homeostasis, ranging from protein and lipid oxidation to glycation and antioxidative capacity. In the present study, the protein, lipid and antioxidant capacity redox homeostasis biomarkers overwhelmingly indicate that, CR, even though not started very early in adulthood, could still offer potential therapeutic effects and it could significantly improve various redox homeostasis biomarkers associated with disease reliably in the heart tissue of aging male Sprague-Dawley rats. Therefore, the effects of CR likely operate through similar mechanisms throughout adulthood and CR seems to have real ameliorative effects on organisms that are not due to confounding factors that come from ad libitum fed rats.

Relation between Endothelial Nitric Oxide Synthase Genotypes and Oxidative Stress Markers in Larynx Cancer.

Nitric oxide synthase (eNOS/NOS3) is responsible for the endothelial synthesis of nitric oxide (NO(•)). G894T polymorphism leads to the amino acid substitution from Glu298Asp that causes lower NOS3 activity and basal NO(•) production in NOS3 894T (298Asp) allele carriers compared with the GG homozygotes. NO(•) acts as an antioxidant protecting against Fenton's reaction which generates highly reactive hydroxyl radicals. Allelic variation of NOS3 may influence an individual's risk of laryngeal cancer (LC). In the current study we have examined the possible relationship between NOS3 G894T genotypes and various systemic oxidative damage markers such as protein carbonyl, advanced oxidation protein products, Cu, Zn-superoxide dismutase, thiol group fractions, and lipid hydroperoxides in LC patients. Genotyping was carried out by PCR-RFLP. In LC patients with TT genotype, Cu, Zn-superoxide dismutase activities and nonprotein thiol levels were significantly higher than the controls. In patients with GT and GG genotype, high levels of lipid hydroperoxides showed statistical significance when compared to controls. Our results indicate a potential relationship among G894T polymorphism of NOS3, and impaired redox homeostasis. Further studies are required to determine the role of NOS3 gene polymorphism and impaired plasma redox homeostasis.