Coenzyme Q10 supplementation affects cellular ionic balance: relevance to aging.

Aging results into disruptive physiological functioning and cellular processes that affect the composition and structure of the plasma membrane. The plasma membrane is the major regulator of ionic homeostasis that regulates the functioning of membrane transporters and exchangers. Coenzyme Q10 is a lipid-soluble antioxidant molecule that declines during aging and age-associated diseases. The present study aims to explore the role of Coenzyme Q10 supplementation to rats during aging on membrane transporters and redox biomarkers. The study was conducted on young and old male Wistar rats supplemented with 20 mg/kg b.w. of Coenzyme Q10 per day. After a period of 28 days, rats were sacrificed and erythrocyte membrane was isolated. The result exhibits significant decline in biomarkers of oxidative stress in old control rats when compared with young control. The effect of Coenzyme Q10 supplementation was more pronounced in old rats. The functioning of membrane transporters and Na+/H+ exchanger showed potential return to normal levels in the Coenzyme Q10 treated rats. Overall, the results demonstrate that Coenzyme Q10 plays an important role in maintaining redox balance in cells which interconnects with membrane integrity. Thus, Coenzyme Q10 supplementation may play an important role in protecting age related alterations in erythrocyte membrane physiology.

Monosodium Glutamate Even at Low Dose May Affect Oxidative Stress, Inflammation and Neurodegeneration in Rats.

Monosodium glutamate (MSG) is a widely used flavour enhancer. A daily intake of MSG at high dosage (2000-4000 mg/kg body weight) is reported to be toxic to humans and experimental animals. The present study aims to investigate the toxic effect of oral administration of MSG at low concentrations (30 and 100 mg/kg body weight) by evaluating biochemical parameters of oxidative stress and inflammation in blood; expression of neuroinflammatory gene and histopathological changes in brain on male Wistar rats. The administration of MSG significantly increases serum level of fasting glucose, insulin, triglycerides, total cholesterol, low-density lipoprotein and decrease level of high-density lipoprotein. Significant low level of FRAP, GSH, SOD, CAT and higher level of MDA, PCO, AOPP, PMRS, NO, CRP, IL-6, TNF-α confirms substantial oxidative stress followed by inflammation after 100 mg MSG treatment. RT-PCR figure shows significant expression of neuroinflammatory gene IL-6 and TNF-α and histopathological examination revealed severe neurodegeneration in hippocampus (CA1 and CA3) and cerebral cortex region of brain at 100 mg MSG treatment. Our result provides evidence that MSG administration at 30 mg does not impose toxicity, however at 100 mg/kg body weight, which is considered a low dose, there is significant toxic effects and may be detrimental to health.

Berberine may provide redox homeostasis during aging in rats.

Aging is a natural phenomenon, which is characterised by progressive physiological changes at cellular and organ level. During aging, the defence mechanism of an organism declines over the period of time. The aim of this study was to investigate the biological efficacy of berberine in D-galactose induced aging rat models. For the study, rats were divided into four groups: Control received only vehicle, BBR received berberine orally, D-Gal received D-galactose subcutaneously and BBR + D-Gal received D-galactose and berberine simultaneously. D-galactose treatment increased the pro-oxidants such as malondialdehyde (MDA) level, protein carbonyl, plasma membrane redox system (PMRS) and advanced oxidation protein products (AOPP) in the erythrocytes or plasma. It reduced the anti-oxidant level such as reduced glutathione (GSH), ferric reducing ability of plasma (FRAP), plasma thiols, sialic acid and membrane transporters like Na+/K+ ATPase and Ca2+ ATPase activity in the erythrocyte membrane. Co-treatment of berberine in D-galactose induced aging rat models restored pro-oxidants and anti-oxidants in erythrocytes. Berberine also restored the activity of Na+/K+ ATPase and Ca2+ ATPase in the erythrocyte membrane. On the basis of these findings, we suggest that berberine treatment could attenuate erythrocyte aging in rats through stabilisation of the redox equilibrium.

Alternate day fasting and time-restricted feeding may confer similar neuroprotective effects during aging in male rats.

Age associated neurodegenerative changes are acknowledged to play a causative role in a majority of neurological diseases that accompany aging in organisms. To alleviate the deteriorative effects of aging in the brain, we investigated the effects oftwo types of intermittent fasting (IF) methods: alternate day fasting (ADF) and time- restricted feeding (TRF) in young (3 months) and old (24 months) in male Wistar rats comparing the results with age matched controls. The evaluation of biomarkers of oxidative stress showed significant decline in the old (ADF and TRF) groups in addition to up regulation in antioxidant levels. It was observed that ADF and TRF methods helped reduce ROS accumulation in the mitochondria and increased the activity of the electron transport chain complexes especially C-I and III. Gene expression analysis of autophagy genes like beclin and LC3B showed upregulated expression in ADF and TRF group. Sirtuin1 expression too significantly increased during fasting in both young and old groups showing fasting induced protection from aging. Histological analysis of sections of cerebral cortex and CA1 area provide evidence that fasting protected neurons against degeneration with age. Our results prompt us to conclude that the efficacy of these fasting methods ADF and TRF are reliable anti- aging strategies with respect to dietary restriction interventions. Moreover, both these methods compete closely in conferring protection from oxidative stress and inducing neuroprotective changes in brain of aged rats when compared to their young counterparts.

Euglena tuba extract provides protection against lipopolysaccharide-induced inflammatory response and oxidative stress in mice.

Lipopolysaccharide (LPS), an endotoxin, is known to induce inflammatory response and oxidative stress in rodents. We evaluated the protective role of Euglena tuba extract (ETME) against LPS induced inflammatory response and oxidative stress in male Balb/c mice. Male Balb/c mice were divided into 4 groups. Group 1 (control) were intraperitoneally administered 0.5 mL PBS. Group 2, 3 and 4 were treated with a single dose of LPS (i.p. 40 mg/kg body weight). Prior 1 h, Group 3 and 4 received orally 100 mg/kg body weight and 200 mg/kg body weight ETME respectively. Biomarkers of oxidative stress including TBARS, SOD, Catalase, Liver marker enzyme (SGPT and SGOT), Nitric Oxide, and inflammatory cytokines including IL-6 and TNF-α, were estimated in serum. Oxidative stress and inflammatory markers were significantly increased in the LPS treated group, whereas ETME treated group at different concentrations protected mice from pro inflammatory cytokines and oxidative stress. Our results indicate that 70% methanolic extract of Euglena tuba can efficiently counteract free radical generation and increased level of inflammatory cytokine in an LPS induced mice model.