ABSTRACT
Nitric oxide (NO) is a gaseous molecule produced from Nitric Oxide Synthases (NOS) enzyme. Three isoforms of NOS have been observed: endothelial NOS (eNOS), inducible NOS (iNOS) and neuronal NOS (nNOS). All three of these isoforms are expressed in liver in varying spatial and temporal ways. In liver, both nNOS and eNOS maintain homeostasis. Whereas iNOS is not expressed constitutively in liver, but rather is expressed in most liver cell types given the appropriate stimulatory conditions. Conflicting results have been observed on the behaviour and possible roles of the NO in several models of ischemia/ reperfusion injury during liver transplantation. Indeed, endogenous NO production has been associated with either protective or cytotoxic effects. Thus some, not all studies suggest that although eNOSderived NO production is protective in ischemia/reperfusion, iNOS derived NO production may contribute to ischemia/ reperfusion injury. This review article focuses on possible role of NO in liver transplantation.
Subject(s)
Humans , Liver/drug effects , Liver/transplantation , Liver Transplantation , Nitric Oxide , Reperfusion Injury/epidemiology , Reperfusion Injury/etiology , Reperfusion Injury/prevention & controlABSTRACT
It has been anticipated that iron and ferritin burden in patients with beta thalassemia major is associated with enhanced free radical formation and blemished antioxidant defense system. The goal of study was to scrutinize impact of serum iron, total iron binding capacity (TIBC), ferritin and erythrocyte catalase in patients with beta thalassemia major. 140 beta thalassemia major patients were studied before and after supplementation of antioxidants for one month, and status was compared with 140 age and sex matched healthy controls. A significant elevation was found in the levels of serum iron and ferritin (P<0.001) with concomitant decrease in erythrocyte catalase (P<0.001) in patients when compared with controls. After one month supplementation of antioxidants, catalase was elevated significantly (P<0.001) and marginal rise in serum TIBC concentration increased marginally while iron and ferritin were decreased marginally (P>0.05) when compared with controls and baselines values. Beta thalassemia major children receive multiple blood transfusions, and are at risk of secondary iron overload induced oxidative stress. These effects may be help to minimize with supplementation of antioxidants.
ABSTRACT
Reactive Oxygen Species (ROS) can induce carcinogenesis via DMA injury. Both enzymatic and non-enzymatic antioxidants participate in cell protection against harmful influence of oxidative stress. The aim of the present study was to assess the level of end product of lipid peroxidation such as malondialdehyde (MDA) as an oxidant in colorectal cancer. Moreover, we analyzed the activity of main non-enzymatic antioxidants, vitamin E and vitamin C in colorectal cancer patients. In the present study, total 48 samples were analyzed which includes 24 age matched healthy controls irrespective of sex (Group I) and 24 cases of colorectal cancer (Group II). The serum level of lipid peroxide, vitamin E and vitamin C were estimated in both healthy control Group I (n=24) and colorectal cancer Group II (n=24). A significant increase in the level of serum lipid peroxide (P<0.001), with concomitant decrease in the levels of serum vitamin E and vitamin C, (P<0.001) in Group II patients were noticed as compared to the healthy control Group I. Our findings suggest that increased oxidative stress and reduced antioxidants defense mechanism may play an important role in progression and pathogenesis of colorectal cancer.