Boron has well-defined biological effects and may be of therapeutic benefit. In the current paper, the effect of
boron in the form of
borax was tested in experimental animal model of
fulminant hepatic failure (FHF). The syndrome was induced in female Wistar rats by three consecutive daily
intraperitoneal injections of
thioacetamide (400 mg/kg). In the treatment groups, rats received
borax (4.0 mg/kg) orally for three consecutive days followed by
thioacetamide. The group administered with
thioacetamide plus vehicle, and the
borax alone treated rats served as controls. In all groups, rats were terminated 4 h after administering the last dose of
thioacetamide, and the tissue/serum was used to measure hepatic levels of
thiobarbituric acid reactive substances,
reduced glutathione, and various
enzymes associated with oxidative stress including
peroxide metabolizing
enzymes and
xanthine oxidase. In
thioacetamide treated group, many fold increase in the activity level of
serum marker enzymes suggesting FHF was observed that could be brought down significantly in rats receiving
boron. Modulation and a correlation in the activity level of
oxidant generating
enzyme and lipid peroxidation as well as hepatic
glutathione level was also observed in rats receiving
thioacetamide. In the group receiving
boron followed by
thioacetamide, these changes could be minimized moderately. The activity level of the
peroxide metabolizing
enzymes and the tripeptide
glutathione, which decreased following
thioacetamide treatment were moderately elevated in the group receiving
boron followed by
thioacetamide. The data clearly shows that
borax partly normalizes the liver and offsets the deleterious effects observed in FHF by modulating the oxidative stress parameters.