Effects of cocaine on oxygen consumption and mitochondrial respiration in normoxic and hypoxic mice
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Primary cultures of rabbit corneal epithelial cells as an experimental model to evaluate ocular toxicity and explore modes of action of toxic injury
2020, Toxicology in VitroCitation Excerpt :Nicotera et al. (1992) has written a review on the role of a disturbance of calcium homeostasis in the cytotoxicity of a number of compounds. LAs have also been shown to have adverse effects on mitochondrial function (Herrmann et al., 1942; Kinoshita, 1959, Dabadie et al., 1987; León-Velarde et al., 1992) and interact with cytoskeletal elements (Haschke et al., 1974; Poste et al., 1975; Dass et al., 1988a, 1988b). Grant and Acosta (1994a) documented LAs produce a dose-dependent increase in toxicity from 60 to 120 min of treatment using the LDH leakage assay and the MTT cytoxicity tests.
Acute effects of cocaine, morphine and their combination on bioenergetic function and susceptibility to oxidative stress of rat liver mitochondria
2013, Life SciencesCitation Excerpt :Furthermore, microarray data suggested that mitochondrial functions and energy metabolism are affected in brains of human cocaine abusers (Lehrmann et al., 2003). Liver mitochondrial bioenergetics was found to be affected by cocaine, since in vivo cocaine administration decreased state 3 respiration and RCR of hepatic mitochondria from rat (Devi and Chan, 1997) and mice (Leon-Velarde et al., 1992), and also decreased the activity of complexes I, II/III, and IV (Devi and Chan, 1997). Importantly, cocaine metabolism may affect its toxicity when administered in vivo, since the cocaine metabolites norcocaine and N–OH–norcocaine are more effective affecting state 3, state 4, RCR, and ADP/O in mitochondria isolated from rat liver, compared to cocaine itself (Boess et al., 2000).
Mitochondrial complex I dysfunction induced by cocaine and cocaine plus morphine in brain and liver mitochondria
2013, Toxicology LettersCitation Excerpt :The increase observed in states 2 and 4 respiration in mitochondria exposed to cocaine suggests an augmentation of the passive transport of H+ into the mitochondria, which is also supported by the increase in respiration observed in the presence of oligomycin, and may be possibly due to a bilateral damage in phospholipids (Videira et al., 2001). Previous studies reported that liver mitochondrial bioenergetics was affected by in vivo cocaine administration, as observed by a decrease in state 3 respiration and RCR of hepatic mitochondria from rats (Devi and Chan, 1997) and mice (Leon-Velarde et al., 1992), and also by a decrease of the activity of complexes I, II/III, and IV (Devi and Chan, 1997). Importantly, cocaine metabolism may also contribute to the effects of in vivo cocaine administration, since the cocaine metabolites norcocaine and N–OH–norcocaine were shown to be more effective affecting state 3, state 4, RCR, and ADP/O in mitochondria isolated from rat liver, compared to cocaine itself (Boess et al., 2000).
Pharmacology and Refraction
2006, Borish's Clinical RefractionEffects of cocaine and its oxidative metabolites on mitochondrial respiration and generation of reactive oxygen species
2000, Biochemical PharmacologyCitation Excerpt :Several studies have suggested that hepatic mitochondria may be an important target for cocaine effects. Significantly diminished state 3 respiration and RCR have been observed in mitochondria isolated from cocaine-treated mice [28] and rats [17]. This impairment of mitochondrial respiration provides a logical explanation for decreased cellular ATP that accompanies hepatotoxic doses of cocaine [14, 29] and perhaps explains, at least in part, loss of cell viability from cocaine both in vivo and in vitro.
Cocaine-induced increase of Mn-SOD in adult rats liver cells
1997, Life Sciences