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Disruption of Mitochondrial Function by Suramin Measured by Rhodamine 123 Retention and Oxygen Consumption in Intact DU145 Prostate Carcinoma Cells¹

William S. Middleton Veteran's Hospital [R. P. R., P. C. B., G. W.], University of Wisconsin Comprehensive Cancer Center [R. P. R., G. W.], and Department of Medicine [P. C. B.], University of Wisconsin Hospitals and Clinics, Madison, Wisconsin 53792

² To whom requests for reprints should be addressed, at University of Wisconsin Comprehensive Cancer Center, K4/666 CSC, 600 Highland Ave., Madison, WI 53792.

Suramin, an antiparasitic drug, has shown antitumor activity in humans. This may occur in part through disruption of energy balance, which is believed to be part of its antiparasitic action. Suramin disrupts mitochondrial function in intact DU145 prostate carcinoma cell monolayers as seen by its causing the release of rhodamine 123 from prestained cells beginning at about 10 µM in 96-well microtiter plates measured with a fluorescent plate scanner. This effect was similar to the ionophore carbonyl cyanide m-chlorophenylhydrazone, dissolved in ethanol at 0.01 N and indicates that suramin acts as a respiratory poison or an ionophore. This effect was confirmed by studies of oxygen consumption with a Clark oxygen electrode and cellular ATP content which demonstrated uncoupling of oxidative phosphorylation by 100 µM suramin, a clinically achievable plasma drug level.

¹ Supported in part by NIH Grant CA-50590 and the Veterans Administration.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Received 9/22/92. Accepted 10/26/92.

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