Journal of Nutritional Disorders & Therapy

Abstract

Antioxidant Enzyme in Blood Test A Marker for Fructose Metabolism

Yamini B Tripathi, Nidhi Pandey and Suyash Tripathi

Excessive fructose consumption can cause metabolic damage. Previous evidence supports that oxidative stress plays a big role in metabolic syndrome (MS)-related manifestations. Recently blood markers like high sensitive-C reactive protein (hs-CRP) and serum lipid profiles are widely used clinical parameters. However, it is unknown if whether antioxidant capacity is related to these changes or not. This study was designed to explore if the concentration of blood markers (triglycerides, cholesterol, glucose, Hs-CRP) is associated to antioxidant capacity in hyperlipidaemia rats. High fructose diet (HFD) was orally given to rats for 80 days to establish hypertriglyceridemia and blood tests were carried on at different time intervals up to 80th day. Serum triglycerides, glucose, glucose, Hs- CRP, SOD, Catalase and LPO were recorded at 50th and 80th days. At last we assessed m- RNA expression of SOD and catalase in WBC. The gradual rise in activities of superoxide dismutase (SOD), catalase and ABTS.+(2,2'- azino-bis(3-ethylbenzothiazoline-6-sulphonic acid)-scavenging potential was recorded without any rise in the serum lipid peroxidation- products, triglycerides (TG), glucose and hs-CRP up to 50th day of HFD feeding. However these changes were reversed on 80th day. The RT-PCR for SOD and catalase mRNA in white blood cells (WBC) also showed similar biphasic. This study suggests that the initial rise in blood antioxidant enzymes to their maximum capability, in early days as adaptive mechanism to encounter the oxidative damage from oxygen free radicals. Thus raised activity of catalase and SOD in blood could be considered as one of the significant biomarkers for early diagnosis of adverse metabolic changes when there is no clinical symptom to MS. This study could be helpful in developing pre-diagnostic parameters to persons, who are likely to develop MS.