Curcumin Attenuates Cr(VI)‐Induced Ascites and Changes in the Activity of Aconitase and F₁F₀ ATPase and the ATP Content in Rat Liver Mitochondria

Abstract

Occupational and environmental exposure to potassium dichromate (K2Cr2O7), a hexavalent chromium compound, can result in liver damage associated with oxidative stress and mitochondrial dysfunction. The purpose of this study was to evaluate the effect of the antioxidant curcumin (400 mg/kg b.w.) on the K2Cr2O7-induced injury, with special emphasis on ascitic fluid accumulation and oxidative phosphorylation mitochondrial enzymes and the adenosine triphosphate (ATP) levels in isolated mitochondria from livers of rats treated with K2Cr2O7 (15 mg/kg b.w.). Thus, curcumin attenuated the ascites generation, prevented the decrease in the activities of aconitase and F1F0 ATPase, and maintained the ATP levels. The activity of complex II was not completely reestablished by curcumin, whereas complexes III and IV activities were unchanged.

Curcumin prevents paracetamol-induced liver mitochondrial alterations

“…To our knowledge, this is the first demonstration that curcumin prevents mitochondrial alteration in the PCM‐induced hepatotoxicity. These data are consistent with the findings in other experimental models . Interestingly, in all cases, the improvement of mitochondrial function was associated with the prevention of the decrease in the activity of aconitase, a marker of oxidative stress .…”

“…The antioxidant curcumin has been found to protect against mitochondrial dysfunction in several experimental models. [ reviewed in ] In potassium dichromate‐induced nephrotoxicity model, curcumin was able to prevent the following mitochondrial alterations: decrease in oxygen consumption, in oxidative stress, in ATP content, in calcium retention, and in mitochondrial membrane potential as well as in the activity of complexes I, II, II‐III and V. In potassium dichromate‐induced hepatotoxicity model, curcumin was able to prevent the decrease in the aconitase activity, in ATP content, in oxygen consumption, and in the activity of respiratory complex I as well as the increase in oxidative stress and in permeability transition pore opening . In maleate‐induced nephrotoxicity model, it was able to prevent reduced oxygen consumption and activities of complex I and aconitase .…”

“…Interestingly, it has not been established whether curcumin may attenuate the following PCM‐induced liver mitochondrial alterations: oxygen consumption, membrane potential, ATP synthesis, and activity of aconitase and respiratory complexes I, II, III and IV. In this context, it has been found that curcumin is able to attenuate mitochondrial alterations in the following experimental models: potassium dichromate‐induced hepatotoxicity and nephrotoxicity, cardiac damage‐induced by chronic renal failure and maleate‐induced nephrotoxicity . By the above mentioned reasons it was hypothesized that curcumin may ameliorate PCM‐induced mitochondrial alterations.…”

Effects of chromium picolinate on fat deposition, activity and genetic expression of lipid metabolism-related enzymes in 21 day old Ross broilers

“…Chromium (Cr) exists in various oxidation states (−2 to +6) [ 1 ], +3 and +6 are the most naturally states in environment [ 2 ]. Hexavalent Cr is more toxic than trivalent [ 3 – 5 ] when measured for genotoxicity, cytotoxicity, and carcinogenicity [ 6 – 8 ].…”

Mitochondrial Biogenesis in Response to Chromium (VI) Toxicity in Human Liver Cells

“…Previous studies indicated that Cr(VI) could cause liver damage through the formation of DNA double-strand breaks and Cr-DNA adducts in the nuclear DNA [ 4 ]. It has also been shown that mitochondrial dysfunction could be caused by Cr(VI) exposure: Cr(VI) could reduce mitochondrial DNA (mtDNA) copy number and inhibit mitochondria electron transport chain complex I, resulting in perturbation of mitochondrial respiration and redox homeostasis [ 8 , 9 ]. These reports indicate that mitochondrion is one of the most sensitive targets of Cr(VI) toxicity.…”