REACTIVE OXYGEN SPECIES INDUCE APOPTOSIS OF SYNOVIOCYTES IN VITRO. α‐TOCOPHEROL PROVIDES NO PROTECTION

Abstract

Reactive oxygen species (ROS) are released during the inflammation of the synovial membrane associated with cartilage degradation in osteoarthritis. In this work, we exposed synoviocytes to superoxide anions at concentrations that may cause either apoptosis or necrosis. We studied membrane organization, dehydrogenase mitochondrial activity and nuclear morphology and integrity, to determine the nature of the death process initiated by superoxide anions and tried to counteract ROS effects with alpha-tocopherol. We found that oxidative stress caused synoviocytes to undergo a process of cell death of an apoptotic nature rather than necrotic. Mitochondrial injury occurred at an early stage, and the FITC-annexin-V-positive/propidium iodide-positive cells occurred later than the metabolic changes. DNA strand breaks were evident at 8 h and nuclear condensation at 24 h. No LDH activity was detected in culture supernatants. In our experimental conditions, alpha-tocopherol had little effect on stress damage; the antioxidant properties of this molecule did not affect the apoptosis caused by superoxide anions.

Oxidative stress in secondary osteoarthritis: from cartilage destruction to clinical presentation?

“…Many studies focused on damaging effects of oxidative and nitrosative agents, 9–11 whereas in the following the differential role of Radical oxygen species (ROS) and radical nitric species (RNS) in osteoarthritis came into focus. A study comparing the effects of nitric oxide and oxidative dysbalance in OA and rheumatoid arthritis postulated a major role of nitric oxide (NO) to modulate chondrocyte function in OA.…”

Effect of vitamin E and menadione supplementation on riboflavin production and stress parameters in Ashbya gossypii

“…It may therefore be inferred that decreased intracellular riboflavin on day 3 in vitamin E cells may be due to increased lipid peroxidation affecting the membranes and causing excretion of riboflavin extracellularly. It is suggested that even at a concentration of 1 mM vitamin E does not prevent membrane damage, but rather would produce alkoxyl radicals than scavenge peroxyl radicals [27]. Vitamin E can act as a prooxidant rather than an antioxidant when co-oxidants such as vitamin C are not available to neutralize the tocopherol radical when oxidative stress is mild [28].…”

Inflammation et réparation tendineuse

“…Lorsqu'ils sont activés, les neutrophiles roulent, puis adhèrent et infiltrent rapidement le site lésé ( Figure 2C, Figure 4A) pour libérer ensuite un arsenal de molécules pro-inflammatoires, parmi lesquelles des chimiokines, des radicaux libres et des protéinases. La libération de radicaux libres de l'oxygène et de l'azote, durant cette phase catabolique, peut entraîner des dommages cellulaires [1], ainsi que l'apoptose des cellules propres au tissu lésé ( Figure 2D) [2]. Il est donc probable que le stress oxydatif puisse provoquer l'apoptose des ténocytes (fibroblastes tendineux) [3] et interférer ainsi avec le processus de réparation du tendon.…”