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Naphthenic acids (NAs) are thought to be a primary cause of toxicity of oil sands process-affected water (OSPW). The purpose of this study was to determine if commercially available adamantane carboxylic acids act by mitrochondrial mechanisms similar to NAs found in OSPW. Mitochondria isolated from rainbow trout (Oncorhynchus mykiss) liver were exposed to commercially available adamantane acids, 3-hydroxyadamantane-1-carboxylic acid (CAS 42711-75-1) and 3,5-dimethyladamantane-1-carboxylic acid (CAS 14670-94-1), or to NAs extracted and purified from OSPW. The effects of these compounds on state 3 and 4 respiration, mitochondrial membrane potential, and mitochondrial reactive oxygen species (ROS; H2O2 production) were quantified. The compound 3-hydroxyadamantane-1-carboxylic acid only inhibited state 3 respiration at the highest concentration (2560 mg/L) and showed a concentration-dependent reduction in H2O2 production. Consistent with extracted OSPW NAs, 3,5-dimethyladamantane-1-carboxylic acid inhibited state 3 respiration and increased H2O2 production, but with a two-fold greater EC50 than the NA mixture extracted from OSPW. All three compounds uncoupled mitochondrial membrane potential and increased state 4 respiration. Based on these results, the adamantane 3,5-dimethyladamantane-1-carboxylic NAs may act via similar mitrochondrial mechanisms as NAs extracted from OSPW and could be used to further explore toxic mechanisms.