Evaluation of the effect of vitamin C on caspase 9 and oxidative stress in rheumatoid arthritis patients

Abstract

Rheumatoid arthritis (RA) is a chronic and an autoimmune disease of the joints and is widely distributed worldwide. It is characterized by alterations of the antioxidant defense system and increased free radical formation and pro-inflammatory cytokine. The aim of the present study was to evaluate the effect of vitamin C supplementation on oxidative stress biomarkers and caspase 9 level in rheumatoid arthritis patients. This study included 30 RA patients and 30 healthy subjects. Plasma levels of malondialdehyde (MDA), total antioxidant capacity (TAC), caspase 9 and 8-hydroxy-2′deoxyguanosine (8 OHdG) were assayed as well as blood vitamin C level. These parameters were reevaluated in RA patients after vitamin C supplementation for one month. Increased MDA and 8 OHdG levels and reduced TAC, caspase 9 and vitamin C. Levels were demonstrated in RA patients. After vitamin C supplementation, RA patients showed significant increase in TAC and vitamin C level and significant decrease in MDA and 8 OHdG levels, plasma caspase 9 level was not significantly affected after vitamin C supplementation. Increased oxidative stress and decreased apoptosis may have an important role in the pathogenesis of RA. The administration of vitamin C supplementation may help to relieve oxidative stress and enhance the antioxidant defense in these patients.

Association of the Adipokines Chemerin, Apelin, Vaspin and Omentin and Their Functional Genetic Variants with Rheumatoid Arthritis

“…A previous study indicated that apelin delayed the onset of apoptosis for a few hours in human enterocyte model (Caco-2), followed by enhanced apoptosis. The antiapoptotic effect of apelin was demonstrated to be as a result of enhanced anti-apoptotic Bcl-2 family proteins synthesis and interaction with phosphatidylinositol 3-kinase protein, whereas its proapoptotic activity may be attributable to suppressed expression of 8-oxoguanine DNA glycosylase1/2 (OGG1/2), DNA oxidative damage repair enzyme, leading to impaired oxidative DNA repair and induction of apoptosis through the mitochondrial apoptotic pathway [74,75]. A previous study reported elevated plasma levels of 8-hydroxy-2 -deoxyguanosine, the cleavage product of OGG enzyme, in RA patients indicating its higher activity to overcome the localized oxidative stress in the RA synovium [76].…”