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³¹P magnetic resonance spectroscopy suggests impaired mitochondrial function in AZT-treated HIV-infected patients

Department of Neurology and The Neuromuscular Research Center, Emory University, Atlanta, GA (Drs. Weissman and Wallace)
Department of Radiology and The Frederik Philips MR Research Center, Emory University, Atlanta, GA (Drs. Weissman, Constantinitis, and Hudgins)
Department of Biochemistry and the Center for Molecular Medicine, Emory University, Atlanta, GA (Dr. Wallace).

Prompted by the report of a mitochondrial myopathy associated with chronic administration of zidovudine (AZT), an inhibitor of mitochondrial DNA synthesis, we obtained ³¹P magnetic resonance spectra from the calf muscles of AZT-treated patients and age-matched control subjects at rest and during an exercise protocol with a 12-second time resolution. The recovery of phosphocreatine following exercise reflects mitochondrial oxidative function and was significantly delayed in the AZT-treated patients (time constants, 43.3 ± 12.5 seconds versus control subjects, 24.4 ± 3.9 seconds). These findings support the hypothesis that the myopathy associated with chronic AZT results from the inhibitory effects of AZT on mitochondrial DNA synthesis and, secondarily, on the inhibition of mitochondrial oxidative metabolism.

Address correspondence and reprint requests to Dr. Joseph D. Weissman, Department of Neurology, Emory University School of Medicine, Woodruff Memorial Building Suite 6000, P.O. Drawer V, Atlanta. GA 30322.

Supported in part by the Emory Medical Care Foundation and the Emory Neuromuscular Center.

Received June 13, 1991. Accepted for publication in final form August 1, 1991.

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