Relationship Between Xanthine Oxidase, Ischemia Modified Albumin, Nitric Oxide with Antioxidants in Non Pregnants, Pre and Post-delivery of Normal Pregnants and Preeclampsia

Abstract

Preeclampsia is a multisystem disorder involves altered homeostasis of oxidants–antioxidants, inflammatory process and endothelial dysfunction. The present study aim was to determine the levels of oxidative stress parameters (malondialdehyde, protein carbonyl, ischemia modified albumin and xanthine oxidase), nutrient antioxidants (vitamin C and vitamin E), enzyme antioxidants (catalase, superoxide dismutase, glutathione peroxidase glutathione reductase), total antioxidant status (TAS) and its association with nitric oxide. The study population consists of three groups, non pregnants (Group 1, n = 57), normotensive pregnants (Group 2, n = 57) and Preeclampsia (Group 3, n = 57). Group 2 and 3 were followed after delivery within 48 h. In preeclampsia xanthine oxidase, malondialdehyde and uric acid levels were significantly increased ( p < 0.001), while TAS decreased ( p < 0.05) when compared to normotensive pregnant and non pregnant. Catalase, glutathione reductase levels were increased ( p < 0.005) and vitamin E, super oxide dismutase levels were decreased ( p < 0.001) in preeclampsia when compared to normal pregnants. Receiver operating characteristics curve analysis showed area under curve for xanthine oxidase (0.8), malondialdehyde (0.804), Uric acid (0.84), ischemia modified albumin (0.92) and catalase (0.88) which indicated as good markers in preeclampsia. Amongst, ischemia modified albumin is a better marker of intrauterine hypoxic reperfusion risk with sensitivity 87.7 % and specificity 91.2 %. The increased hydrogen peroxide from xanthine oxidase adds to oxidative stress and increased catalase activity in preeclampsia represents combating action. Increased oxidative stress, decreased TAS and its apparent reversible changes evinced within 48 h after delivery in preeclampsia illustrated that placental abnormality is the contributing factor in the pathogenesis.