Impaired redox status and cytochrome c oxidase deficiency in patients with polymyalgia rheumatica.

Objective: To evaluate redox status and muscular mitochondrial abnormalities in patients with polymyalgia rheumatica (PMR).

Methods: Prospective evaluation of deltoid muscle biopsy in 15 patients with PMR. Fifteen subjects matched for age and sex, with histologically normal muscle and without clinical evidence of myopathy, were used as controls.

Cytochrome c oxidase deficiency in the muscle of patients with zidovudine myopathy is segmental and affects both mitochondrial DNA- and nuclear DNA-encoded subunits.

Zidovudine (AZT) can induce a mitochondrial disorder associated with mitochondrial (mt) DNA depletion affecting skeletal muscle, heart, and liver. Zidovudine myopathy is characterized by ragged-red fibers and partial cytochrome c oxidase (COX) deficiency. We evaluated at a single fiber level the expression of COX II (mtDNA-encoded) and COX IV (nuclear DNA-encoded) subunits in 12 HIV-infected patients with zidovudine myopathy.

Influence of handling procedures on rat plasma creatine kinase activity.

Ten-week-old Sprague-Dawley rats were held behind the front legs before and during anesthetic injection of sodium pentobarbital (group 1, 12 rats), or lifted by the base of the tail before and during injection (group 2, 12 rats). Creatine kinase (CK) values were higher (P = 0.004) in group 1 (median 564 IU/L) than in group 2 (median 272 IU/L).