Contact: Dr. Robert K.M. KO (PhD, UBC, 1990)
Assistant Professor
E-Mail ---->
bcrko@usthk.ust.hk
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Free radical-related mechanisms in tissue injuries, especially
myocardial ischemia/reperfusion injury and carbon tetrachloride-induced
hepatotoxicity; protection against such injuries by antioxidants;
transition metal ions and hydroperoxide-mediated peroxidation of
biological membrane lipids;
age-related alterations in tissue antioxidant defence;
antioxidant properties of traditional Chinese medicinals in relation to
their anti-aging activities; isolation of active principle(s) from
Chinese medicinals; fractionation of their pharmacologically active
components; HPLC and centrifugal partition chromatography.
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Medline. At the National Institutes of Health.
Medline.At Healthgate.
Ko K.M., Ip S.P., Poon M.K.T., Wu S.S., Che C.T., Ng K.H., Kong Y.C.,
"Effect of a lignan-enriched Fructus Schisandrae extract on hepatic
glutathione status in rats: Protection against carbon tetrachloride toxicity."
Planta Med. 61:134-137, 1995.
Ko KM; Yick PK; Poon MK; Ip SP
Prooxidant and antioxidant effects of Trolox on ferric ion-induced oxidation of erythrocyte membrane lipids.
Department of Biochemistry, Hong Kong University of Science and Technology, Clear Water Bay, Kowloon.
Mol Cell Biochem, 1994 Dec 7, 141:1, 65-70
The prooxidant and antioxidant actions of Trolox were examined in an in vitro system measuring ferric ion-induced oxidation of erythrocyte membrane
lipids. Trolox was found to produce a concentration-dependent biphasic effect on the ferric ion-stimulated lipid peroxidation, with the mode of action
being similar to those produced by reducing-agent antioxidants, such as ascorbic acid and reduced glutathione, and iron chelator, such as
desferrioxamine. Phytic acid, a potent iron chelator, could suppress the prooxidant actions of Trolox and desferrioxamine, but not those of ascorbic
acid and reduced glutathione. The ability of Trolox to stimulate ferric ion-catalyzed ascorbate oxidation, as similar to the action produced by
ethylenediaminetetraacetic acid, indicates the presence of iron-chelating activity. The ensemble of results suggests the possible involvement of iron
chelation in the prooxidant action of Trolox in ferric ion-stimulated lipid peroxidation reactions.
Unique Identifier
95183053
Ip S.P., Poon M.K.T., Wu S.S., Che C.T., Ng K.H., Kong Y.C. and Ko K.M.
Effect of schisandrin B on hepatic glutathione antioxidant system in mice:
protection against carbon tetrachloride toxicity.
Department of Biochemistry, Hong Kong University of Science & Technology, Clear Water Bay, Kowloon.
Planta Med, 1995 Oct, 61:5, 398-401
Pretreating female Balb/c mice with schisandrin B (Sch B) at increasing daily doses (1-4 mmol/kg) for 3 days caused dose-dependent increases in hepatic glutathione S-transferase (GST) and glutathione reductase (GRD) activities. However, the activities of glucose-6-phosphate dehydrogenase (G6PDH), Se-glutathione peroxidase (GPX), and gamma-glutamylcysteine synthetase (GCS) were down-regulated to varying degrees in a dose-dependent manner. While there were biphasic changes in hepatic reduced glutathione (GSH) level as well as susceptibility of hepatic tissue homogenates to in vitro peroxide-induced GSH depletion, a gradual decrease in hepatic malondialdehyde content was observed. The beneficial effect of Sch B on the hepatic GSH anti-oxidant system became more evident after CCl4 challenge. The same Sch B pretreatment regimen caused a dose-dependent protection against carbon tetrachloride (CCl4)-induced hepatotoxicity. The hepatoprotection was associated with significant enhancement in hepatic GSH status, as indicated by the substantial increase in tissue GSH levels and the corresponding decrease in susceptibility of tissue homogenates to GSH depletion. Where the activities of GST and GRD were increased linearly over non-CCl4 control values, there was also a gradual elevation in G6PDH activity upon administration of increasing doses of Sch B. In contrast, GPX activity was moderately down-regulated. The ensemble of results suggests that the hepatoprotection afforded by Sch B pretreatment may mainly be attributed to the enhancement in the functioning of the hepatic GSH anti-oxidant system, possibly through stimulating the activities of GSH related enzymes.
Ko K.M., Duncan H.F. Mak, Li P.C., Poon M.K.T. and Ip S.P.
Protective effect of a lignan-enriched extract of Fructus Schisandrae
on physical exercise induced muscle damage.
Phytotherapy Res. (in press)
Ko K.M., Duncan H.F. Mak, Li P.C., Poon M.K.T. and Ip S.P.
Enhancement of hepatic glutathione regeneration
capacity by a lignan-enriched extract of Fructus Schisandrae in rats.
Jpn J Pharmacol. (in press)
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