IN VIVO EVALUATION OF THE ROLE OF D-RIBOSE-L-CYSTEINE IN ACETAMINOPHEN- INDUCED LIVER DAMAGE USING WISTAR RAT

Doris Nnenna Ajibo*, Akpotu Emamuzou Ajirioghene, Emem John Offong, Silver Isosiya Davies, Akpan Godwin Williams and Okwubie Lambert

ABSTRACT

Acetaminophen- induced hepatotoxicity is usually provoked by oxidative stress. D-ribose-L-cysteine (DRLC) is a precursor in the synthesis of glutathione (GSH). It minimizes oxidative stress. Experimental animals were grouped into 4(n=5). Group1received control (10mg/kg), group 2 received Acetaminophen 150mg/kg and DRLC 125mg/kg, group 3 received Acetaminophen 150mg/kg and DRLC 250 mg/kg while group 3 received Acetaminophen alone at 150mg/kg. The level of Glutathione level (GSH), Malondialdehyde (MDA), Catalase (CAT), Nitric oxide (NO), C-reactive protein (CRP) and Gamma glutamyl transferase (GGT) were analyzed. Administration of DRLC at both doses (125 and 250 mg/kg) post treatment with acetaminophen (150mg/kg), significantly elevated the hepatic level of GSH, GSH-Px and CAT in experimental rats compared to control. Lipid peroxidation was minimized seen with a decrease in the hepatic level of MDA. Liver GGT was also reduced whereas administration of Acetaminophen (150mk/kg) alone reduced the level of GSH, GSH-Px and CAT. However, there were no significant differences in the level of NO and C-reactive protein (CRP) of both the DRLC 125mg/kg and 250mg/kg compared to the control. Therefore, this investigation suggests that DRLC both at 125mg/kg and 250mg/kg mitigates acetaminophen-induced hepatotoxicity.

Keywords: Acetaminophen, D-ribose-L-cysteine (DRLC), Glutathione, Oxidative stress.