In: General Physiology and Biophysics, vol. 37, no. 1
Oľga Otrubová - Ladislav Turecký - Oľga Uličná - Pavol Janega - Ján Luha - Jana Muchová
Rok, strany: 2018, 23 - 31
N-acetyl-L-cysteine (NAC) is a drug routinely used in several health problems, e.g. liver damage. There is some information emerged on its negative effects in certain situations. The aim of our study was to examine its ability to influence liver damage induced by long-term burden. We induced liver damage by CCl4 (10 weeks) and monitored the impact of parallel NAC administration (daily 150 mg/kg of b.w.) on liver morphology and some biochemical parameters (triacylglycerols, cholesterol, alanine aminotransferase (ALT), aspartate aminotransferase (AST), bilirubin, bile acids, proteins, albumins and cholinesterase). NAC significantly decreased levels of bile acids and bilirubin in plasma and triacylglycerols in liver, all of them elevated by impairment with CCl4. Reduction of cholesterol induced by CCl4 was completely recovered in the presence of NAC as indicated by its elevation to control levels. NAC administration did not improve the histological parameters. Together with protective effects of NAC, we found also its deleterious properties: parallel administration of CCl4 and NAC increased triacylglycerols, ALT and AST activity and significantly increased plasma cholinesterase activity. We have observed nonsignificantly increased percentage of liver tissue fibrosis. Our results have shown that NAC administered simultaneously with liver damaging agent CCl4, exhibits not only protective, but also deleterious effects as indicated by several biochemical parameters.
Otrubová, O., Turecký, L., Uličná, O., Janega, P., Luha, J., Muchová, J. 2018. Therapeutic effects of N-acetyl-L-cysteine on liver damage induced by long-term CCl4 administration. In General Physiology and Biophysics, vol. 37, no.1, pp. 23-31. 0231-5882.
Otrubová, O., Turecký, L., Uličná, O., Janega, P., Luha, J., Muchová, J. (2018). Therapeutic effects of N-acetyl-L-cysteine on liver damage induced by long-term CCl4 administration. General Physiology and Biophysics, 37(1), 23-31. 0231-5882.