Abstract
BackgroundPhenylhydrazine, a hemolytic agent, is widely used as a model of experimental hyperbilirubinemia. Palm tocotrienol-rich fraction (TRF) was shown to exert beneficial effects in hyperbilirubinemic rat neonates.AimTo investigate the effects of palm TRF supplementation on hepatic bilirubin-metabolizing enzymes and ocidative stress status in rats administered phenylhydrazine.MethodsTwenty-four male Wistar rats were divided into two groups; one group was intraperitoneally injected with palm TRF at the dose of 30 mg/kg/day, while another group was only given vehicle (control) (vitamin E-free palm oil) for 14 days. Twenty-four hours after the last dose, each group was further subdivided into another two groups. One group was administered phenylhydrazine (100 mg/kg, intraperitoneally) and another group was administered normal saline. Twenty-four hours later, blood and liver were collected for biochemical parameter measurements.ResultsPhenylhydrazine increased plasma total bilirubin level and oxidative stress in the erythrocytes as well as in the liver, which were reduced by the pretreatment of palm TRF. Palm TRF also prevented the increases in hepatic heme oxygenase, biliverdin reductase and UDP-glucuronyltransferase activities induced by phenylhydrazine.ConclusionPalm tocotrienol-rich fraction was able to afford protection against phenylhydrazine-induced hyperbilirubinemia, possibly by reducing oxidative stress and inhibiting bilirubin-metabolizing enzymes in the liver.
Highlights
Phenylhydrazine is a strong oxidant agent, which is extensively used in industries, laboratories and therapeutics [1]
Phenylhydrazine-induced hemolysis increases the formation of bilirubin [6] and would affect the enzymes that are involved in the bilirubin metabolism
Another enzyme involved in the bilirubin metabolism is aminolevulinic acid synthase which is affected by the increased heme production [8]
Summary
Phenylhydrazine is a strong oxidant agent, which is extensively used in industries, laboratories and therapeutics [1]. Phenylhydrazine-induced hemolysis increases the formation of bilirubin [6] and would affect the enzymes that are involved in the bilirubin metabolism. A degradation product of hemolysis will be oxidized and converted into biliverdin by heme oxygenase, a rate-limiting enzyme for bilirubin synthesis. Biliverdin is reduced to bilirubin by biliverdin reductase before being conjugated to glucuronides by UDP-glucuronyltransferase in the liver [7]. Another enzyme involved in the bilirubin metabolism is aminolevulinic acid synthase which is affected by the increased heme production [8]. Phenylhydrazine was shown to increase aminolevulinic acid synthase [8] and heme oxygenase activities in the rat liver [9]. Palm tocotrienol-rich fraction (TRF) was shown to exert beneficial effects in hyperbilirubinemic rat neonates
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