Oxidative Stress

Hypertension is a common disease and is an important cause of morbidity and mortality worldwide. Occurrence of oxidation and peroxidation is one of the unfavorable consequences of hypertension on molecular systems. Large epidemiologic studies have demonstrated that subjects with hypertension have a marked increase in the prevalence of hypercholesterolemia, diabetes, hypomagnesemia, hypertriglyceridemia.  Paraoxonase1(PON1),an HDL bounded enzyme, protects LDL from oxidative stress by destroying biologically active phospholipids . Human serum PON1 activity was shown to be inversely related to the risk of cardiovascular diseases, and low PON1 activities were observed in atherosclerotic, hypercholesterolemic and hypertensive patients .

A study was undertaken to assess both oxidative stress and inflammation in the lungs of patients with chronic obstructive pulmonary disease (COPD) during mild, chronic, severe and acute exacerbations compared with those with stable COPD, healthy smokers, and non-smokers. Levels of interleukin 8 (IL-8) were measured as markers of airway inflammation and TAS levels were measured as a marker of antioxidant status. MDA levels were measured as a marker of oxidative stress status in the serum of COPD patients. Mean serum MDA levels and levels of IL-8 were significantly high in COPD patients and mean serum antioxidant levels were significantly low in patients as compared to non COPD control. It was further observed that the level of MDA and IL8 elevates while that of total antioxidant level falls with the increase in Gold stage and number of smoking pack years amongst the study subjects. Oxidative stress possibly have role in the pathogenesis of COPD and its complications as indicated by the enhanced levels of lipid peroxidation product malondialdehyde and IL-8 in patients. The lower levels of the antioxidant enzyme status point towards that altered antioxidant defense system in patients. Antioxidant therapeutic use and IL-8 antagonists may have clinical usefulness in the treatment of COPD and in preventing its complication and recurrent exacerbations which may improve disease outcome.

Alcohol withdrawal (AWD) is characterized by signs of major oxidative stress and the loss of neural cells. The present study was designed to investigate the role of the total aqueous extract from rhizomes of ginger on ethanol withdrawal related oxidative stress and related damage  in brain regions of rat. α- Lipoic acid (ALA) (100 mg/kg b.w., i.p.) was used as a standard drug. Silymarin (100 mg/kg b.w., o.p.), a well known antioxidant was used for comparision. The ginger extract improved the level of protective antioxidants such as glutathione peroxidase (GPx), reduced glutathione (GSH), glutathione reductase (GRD), superoxide dismutase (SOD) and catalase (CAT) and inhibited XOD activity in the brain regions under study at a dose of 200 mg/kg, p.o. compared to silymarin or ALA or both combined. Moreover, a decline in the antioxidant enzyme level was observed during chronic ethanol administration too (20% ethanol @ mg/kg, p.o.). Interestingly, significant improvement was recorded with the supplementation of ginger extract by an improvement of the antioxidant enzyme status even in rats with chronic ethanol administration. In addition, a striking difference is observed in the decline in absorbance at 540 nm that reflects mitochondrial PTP opening of rats treated with ginger extract during chronic ethanol administration and ethanol withdrawal compared to rats that are subjected to the identical stress but without extract treatment. The current results indicate the possible utility of ginger rhizome in neuroprotection against neurodegenerative alcohol associated disorders such as ethanol withdrawal.