Liposomal curcumin may be useful for the prevention of copper sulphate induced liver injury. - GreenMedInfo Summary
Liposomal Curcumin Attenuates the Incidence of Oxidative Stress, Inflammation, and DNA Damage Induced by Copper Sulfate in Rat Liver.
Dose Response. 2018 Jul-Sep;16(3):1559325818790869. Epub 2018 Aug 9. PMID: 30116168
Background: Copper is an essential element that is used widely in agriculture as fungicides and insecticides; for example, it is used to control schistosomiasis and as an antiseptic and germicide. Copper sulfate (CuSO) induces multiorgan dysfunction through the stimulation of reactive oxygen species and oxidative stress. Despite the numerous pharmacological effects of curcumin (CUR), its pharmacokinetic properties are less promising. Hence, there is an urgent need for novel, effective strategies to attenuate heavy metal toxicity and consequently improve the treatment efficiency. Liposomal curcumin (L-CUR) improves the dissolution, stability, and bioavailability of treatment agents. This study compared the efficacy of CUR and L-CUR with that of desferrioxamine (DES), which is a heavy metal chelator against CuSOhepatotoxicity.
Methods: All treatments with the aforementioned antioxidants were administered for 7 days along with CuSO. Serum levels of alanine aminotransferase, aspartate transaminase, lactate dehydrogenase, and C-reactive protein, hepatic nitric oxide (NO), and lipid peroxides (malondialdehyde) were measured; protein expression of cyclooxygenase 2 and DNA fragmentation were evaluated. Histopathological examinations were also conducted.
Results: A toxic dose of CuSOinduced elevations in the previously measured parameters;, whereas glutathione (GSH) and superoxide dismutase (SOD) levels were decreased. Treatment with the antioxidants in question modulated these levels. Liposomal CUR has more hepatoprotective efficiency than CUR, and its efficacy was similar to that of DES. The histopathological examinations confirmed these results.
Conclusions: Liposomal CUR may be useful for the prevention of CuSO-induced liver injury. Cyclooxygenase 2 protein expression and DNA fragmentation were involved in CuSOtoxicity and treatment.