Caffeic acid phenyl ester prevents cadmium intoxication induced disturbances in erythrocyte indices and blood coagulability, hepatorenal dysfunction and oxidative stress in rats

Abstract

Here we investigated the protective role of caffeic acid phenyl ester (CAPE) on erythrocyte indices and osmotic resistance, blood coagulation, hepato-renal function and antioxidant status in cadmium (Cd) toxicity in rats. Cd intoxication was induced by intraperitoneal injection (i.p.) of cadmium chloride (1mg/kg/day) for 21 days, and CAPE was daily given (10μmol/kg; i.p.) also for 21 days. At day 22, blood samples, livers and kidneys were prepared for screening of: (1) erythrocyte indices: red blood cell (RBC) count, osmotic fragility, hemoglobin (HGB) concentration, hematocrit (HCT), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC); (2) blood coagulation tests: prothrombin time (PT), activated partial thromboplastin time (APTT), and fibrinogen (FIB) level; (3) serum levels of liver and kidney function biomarkers (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, albumin, creatinine and blood urea nitrogen); (4) blood, liver and kidney levels of Cd; and (5) serum and hepato-renal concentrations of glutathione (GSH), superoxide dismutase (SOD), and thiobarbituric acid reactive substances (TBARS). Cd intoxication significantly impaired hepato-renal function, prolonged PT and APTT, reduced FIB, decreased RBC count and osmoresistnacy as well as the values of HGB, HCT, MCV, MCH and MCHC. Interestingly, therapy with CAPE successfully eliminated Cd and significantly stabilized erythrocyte indices, blood coagulability and hepato-renal functional status in Cd-intoxication. Additionally, CAPE therapy significantly reversed the decreases in GSH and SOD, and the increases in TBARs that were induced by Cd intoxication. In conclusion, CAPE can represent a promising therapeutic agent in eliminating Cd and counteracting its hematological, hemostasis and hepatorenal toxic effects.