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Prolonged aldosterone administration to mice was investigated in relation to liver function. Daily injections of 2 µg. d-aldosterone monoacetate/g. body weight for 60 days adversely affected oxidative phosphorylation of liver mitochondria. The value for the P:O ratio of controls, 3·21, dropped to 2·01, 2·86, 2·45 and 2·79 for mice treated with aldosterone for 20, 30, 50 and 60 days, respectively. The impaired oxidative phosphorylation was neither accompanied by an increase in adenosine triphosphatase activity of liver mitochondria nor by a change in plasma transaminases. Corresponding morphological changes were observed in liver parenchyma starting with hydropic degenerations in early lesions, and single cell necrosis accompanied by mitotic activity (regeneration) in advanced lesions. It seems therefore that hyperaldosteronism might be noxious to liver parenchyma and hepatic function.