A reciprocal relationship between mitochondria and lipid peroxidation determines the chondrocyte intracellular redox environment.

ABSTRACT: In orthopedic research, many studies have applied vitamin E as a protective antioxidant or used tert-butyl hydroperoxide to induce oxidative injury to chondrocytes. These studies often support the hypothesis that joint pathology causes oxidative stress and increased lipid peroxidation that might be prevented with lipid antioxidants to improve cell survival or function and joint health; however, lipid antioxidant supplementation was ineffective against osteoarthritis in clinical trials and animal data have been equivocal. Moreover, increased circulating vitamin E is associated with increased rates of osteoarthritis. This disconnect between benchtop and clinical results led us to hypothesize that oxidative stress-driven paradigms of chondrocyte redox function do not capture the metabolic and

SUBMITTER: Hines MR 

PROVIDER: S-EPMC11366903 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature