The effect of caffeic acid phenethyl ester (CAPE) on cadmium-induced liver damage in mice
TL;DR
Under the experimental conditions used, CAPE attenuated cadmium-associated increases in serum ALT and AST, and the absence of a vehicle-only injected control prevents the higher TOS in the CAPE group from being attributed specifically to CAPE rather than to the DMSO vehicle or injection procedure.
Abstract
This study assessed the effect of caffeic acid phenethyl ester (CAPE) on serum biochemical changes during cadmium chloride exposure in mice. Twenty-four male Mus musculus were randomly assigned to four groups (n=6 each): control, CAPE, cadmium chloride, and cadmium chloride+CAPE. CAPE (10 µmol/kg/day) and cadmium chloride (1 mg/kg/day) were administered intraperitoneally for seven days. Serum total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), total thiol, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were evaluated. TOS differed among groups (F=5.993; p=0.004), driven by a higher value in the CAPE group than in controls (p=0.003). TAS, OSI, and total thiol did not differ significantly (p=0.808, p=0.857, and p=0.410, respectively). Cadmium chloride increased ALT from 24.34±1.09 to 55.85±3.48 U/L and AST from 91.41±1.31 to 187.30±3.76 U/L. Co-administration of CAPE reduced these activities to 34.35±2.34 and 138.60±2.82 U/L, respectively (both p<0.001 vs cadmium chloride), although values remained above control levels. Under the experimental conditions used, CAPE attenuated cadmium-associated increases in serum ALT and AST. This observation is limited to the biochemical parameters measured and does not establish histological or mechanistic hepatoprotection. The absence of a vehicle-only injected control prevents the higher TOS in the CAPE group from being attributed specifically to CAPE rather than to the DMSO vehicle or injection procedure.