Tumor Marker Enzymes Research Articles

Anticancer potency of the milk extract of Semecarpus anacardium Linn. nuts against aflatoxin B1 mediated hepatocellular carcinoma bearing Wistar rats with reference to tumour marker enzymes.

Aflatoxin B1 is an important consideration in the aetiology of human and animal hepatocellular carcinoma. The influence of the drug, Semecarpus anacardium Linn. nut extract, on hepatocarcinogenicity of aflatoxin B1 was evaluated in adult albino male Wistar rats. Aflatoxin B1 was administered intraperitoneally to induce hepatocellular carcinoma. These cancer bearing animals were treated with Semecarpus anacardium Linn. nut extract (200 mg/kg body weight/day) in sunflower oil orally for 14 days. The plasma and the liver tumour tissue were investigated biochemically for lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and gamma-glutamyl transpeptidase. The elevation of plasma concentration of these enzymes were indicative of the persistent deteriorating effect of aflatoxin B1 in cancer bearing animals. Lactate dehydrogenase and aminotransferases levels were decreased in liver, whereas alkaline phosphatase and gamma-glutamyl transpeptidase were increased in cancer conditions. These enzyme levels were reversed to near normal control values in drug treated animals. The analysis of marker enzyme activities clearly indicates the antitumour efficacy of Semecarpus anacardium Linn. nut extract on aflatoxin B1 induced hepatocellular carcinoma.

DIETARY CURCUMIN WITH CISPLATIN ADMINISTRATION MODULATES TUMOUR MARKER INDICES IN EXPERIMENTAL FIBROSARCOMA

Curcumin, the active constituent ofCurcuma longa, which itself possesses antitumour activity against experimental tumours, enhances the antitumour effect of the widely used anticancer drug cisplatin, when used in combination against fibrosarcoma. Tumour marker enzymes such as aminotransferases, lactate dehydrogenase, γ-glutamyl transpeptidase, alkaline phosphatase, 5′-nucleotidase were analysed in liver and kidney homogenates of experimental rats. All these enzyme activities were markedly increased in tumour bearing animals. On cisplatin administration, the enzyme levels were decreased but not to near normal values. Curcumin, when treated along with cisplatin brought back the enzyme levels to near the control values. Thus curcumin and cisplatin combination may be worth trying against tumours like fibrosarcoma.

The salubrious effect of tamoxifen [correction of Tamaxifen] on serum marker enzymes, glycoproteins, and lysosomal enzymes level in breast cancer woman.

Tumour markers correlate strongly with prognosis based on tumour burden and surgical resectability. If chemotherapy is extremely effective in certain stage of the disease, the sensitive marker may be of great use in monitoring disease response and drug treatment. Hence, this study was launched to evaluate the changes in tumour marker enzymes like lactate dehydrogenase (LDH), glutamate oxaloacetate transaminase (SGOT), glutamate pyruvate transaminase (SGPT), alkaline phosphatase, and acid phosphatase in before and after 3 and 6 months tamoxifen treated breast cancer patients. In addition, the changes in serum glycoproteins viz., hexose, hexosamine, and sialic acid and lysosomal enzymes such as N-acetyl-beta-D-glucosaminidase, beta-D-galactosidase, and beta-D-glucuronidase were analysed in these patients. These values were compared with their age matched healthy control subjects. At 6 months evaluation, the tamoxifen treated postmenopausal breast cancer women showed a statistically significant decreased (p < 0.001, 0.05 respectively) levels of LDH, SGOT, SGPT, alkaline and acid phosphatases than their baseline values. Similarly, the levels of hexose, hexosamine, and sialic acid and N-acetyl-beta-D-glucosaminidase, beta-D-galactosidase, and beta-D-glucuronidase were decreased significantly (p < 0.001) in tamoxifen received postmenopausal women. The result of this study suggested that tamoxifen potentially retard the metastasis of breast cancer as well as the bone demineralisation in postmenopausal breast cancer women. Thus, tamoxifen may also have its antitumour activity through its beneficial effects on tumour marker enzymes and serum proteins in breast cancer women.

Different starting times of α-tocopherol and γ-tocotrienol supplementation and tumor marker enzyme activities in-the rat chemically induced with cancer

1. 1. α-Tocopherol (α-T) and γ-tocotrienol (γ-T) were supplemented continuously for 8 weeks in the diets of normal rats and rats chemically induced with cancer using diethylnitrosamine (DEN), 2-acetylaminofluorene (AAF) and partial hepatectomy. Hepatocarcinogenesis was followed by determining the plasma γ-glutamyl-transpeptidase (GGT) and alkaline phosphatase (ALP) activities as well as placental glutathione S-transferase (PGST) and GGT activities histochemically, at 4-week intervals. 2. 2. Male Rattus norvegicus were supplemented α-T and γ-T at two different doses of 30 and 300 mg/kg diet. The supplementation was started at three different times: simultaneously with DEN administration; 4 weeks; and 8 weeks after DEN administration. 3. 3. Elevation of plasma GGT activities and formation of PGST and GGT positive foci were attenuated significantly ( P< 0.05) when α-T and γ-T were supplemented simultaneously with cancer induction. Supplementation begun 4 and 8 weeks after cancer induction did not affect plasma enzyme activities and formation of enzyme-positive foci. 4. 4. α-T was more effective than γ-T, and a lower dose of 30 mg/kg was found to be more effective in reducing the severity of hepatocarcinogenesis.

Effect of ovariectomy and sex hormones replacement on tumour marker enzymes under administration of chemical carcinogens in the rat

The effect of ovariectomy and sex hormone/s replacement in female rats was investigated by the determination of the tumour marker enzymes gamma-glutamyltranspeptidase (GGT) and alkaline phosphatase (ALP). This was compared to ovariectomized rats receiving sex hormone replacement and treated with carcinogen. Ovariectomy significantly increased the activity of plasma GGT. Plasma and microsomal ALP and microsomal GGT were unchanged. When replacements of estrogen (E), or progesterone (Prog), or combinations of both estrogen and progesterone were given to ovariectomized rats, the activity of plasma GGT was brought to the level of normal intact females. Treatment with carcinogen increased the PGGT activities in intact rats. In ovariectomized rats receiving carcinogen, the PGGT activities were significantly lower than in intact females and rats receiving both hormone replacement and carcinogen (p < 0.01). Carcinogen treatment in case of estrogen or progesterone replacement, either individually or in combination, showed GGT activities comparable to intact females receiving carcinogen. Both plasma and microsomal ALP were not affected by carcinogen administration. These results showed that ovariectomy reduced the severity of hepatocarcinogenesis while sex hormone replacement worsened the process.

Effect of .GAMMA.-Tocotrienol and .ALPHA.-Tocopherol on Blood Glutathione and Tumor Marker Enzymes during Chemical Hepatocarcinogenesis in the Rat.

The protective effect of two types of vitamin E (α-tocopherol and γ-tocotrienol) in rats treated with diethylnitrosamine (DEN) and 2-acetylaminofluorene (AAF) were studied by determination of plasma alkaline phosphatase (ALP), plasma and liver microsomal γ-glutamyl transpeptidase (GGT) activities, and blood glutathione (GSH). Rats treated with DEN/AAF had significantly elevated plasma and microsomal GGT, plasma ALP activities, and blood GSH levels compared with the normal controls (p<0.05). Supplementation with vitamin E of normal controls did not affect the enzyme activities or blood GSH. In rats treated with DEN/AAF, vitamin E supplementation attenuated GGT and ALP activities and blood GSH levels. The optimum dose required for highest attenuation of the tumor marker enzyme activities was 34mg/kg diet for α-tocopherol and 30mg/kg diet for γ-tocotrienol. Higher doses of the vitamin did not show further attenuation in the level of the tumor marker enzyme activities.

Effects of female sex steroids on concanavalin A-mediated agglutination of hepatocytes from nonregenerating and regenerating rat liver and hepatic tumor marker enzymes.

Effect of treatment of female rats with an oral contraceptive agent (OCA), Ovulen-50, for 7 weeks on agglutination of hepatocytes with concanavalin A (con A) and activities of certain tumor marker enzymes were examined to find out if OCA treatment is related to preneoplastic or neoplastic processes. Hepatocytes from regenerating and nonregenerating livers of control female rats showed negligible agglutination with Con A, whereas hepatocytes from non regenerating but not from the regenerating livers of female rats treated with a combination of 5 micrograms ethinyl estradiol and 100 micrograms ethynodiol diacetate showed agglutination. Of the tumor marker enzymes such as hepatic glucose 6-phosphatase, gamma-glutamyl transpeptidase (gamma-GT), and arginase examined in the liver, only gamma-glutamyl transpeptidase showed a significant increase in activity in the steroid-treated rats. Plasma alkaline phosphatase activity was also higher in the treated animals. However, the magnitude of the changes observed was relatively small and perhaps unrelated to the neoplastic process.