摘要:

Levels of activity of the enzyme aryl hydrocarbon hydroxylase and cytochrome P450 have been estimated in lung and liver of rats exposed to graded doses of cigarette smoke and in human bronchial mucosa of smokers, non-smokers and patients with lung cancer. Exposure of rats to smoke of four cigarettes increased both hepatic and pulmonary aryl hydrocarbon hydroxylase activity. Exposure to smoke of four cigarettes daily for seven and 14 days did not result in higher aryl hydrocarbon hydroxylase levels in the liver than one day’s exposure, but in the lung longer exposures caused greater increases in enzyme activity. Injection of benzo(a)pyrene at two dose levels caused a much greater increase in both liver and lung aryl hydrocarbon hydroxylase than smoking. The lower dose maximally stimulated the enzyme in both organs. The changes in aryl hydrocarbon hydroxylase activity were accompanied by significant increases in both liver weight and the cytochrome P450 content of liver microsomes but the increase in cytochrome P450 did not parallel those in aryl hydrocarbon hydroxylase activity. Of 40 surgical and autopsy specimens of human lung and tracheal mucosa from smokers, non-smokers and cancer patients, only one was found to have detectable aryl hydrocarbon hydroxylase activity. The relationship between aryl hydrocarbon hydroxylase induction by cigarette smoke in human tissues and the development of bronchogenic carcinoma in smokers remains unclea

ISSN:0030-2414    

DOI:10.1159/000225143

出版商:S. Karger AG    

年代:1976

数据来源: Karger

摘要:

Inhibition of mouse hepatic aryl hydrocarbon hydroxylases (AHH), microsomal mixed-function oxidases was obtained with five bivalent metal chlorides. Concentrations ranged from 10––6 to 10––1 m. The enzyme system was induced by an intraperitoneal injection of a trioctanoin solution of 3-methylcholanthrene into C57B1/6J mice 24 hours before the hepatic AHH was measured. Activity was calculated as: ng of 3-hydroxybenzo(a)pyrene formed in 20 min at 37°C per mg of protein. Cadmium was the most inhibitory of the metals tested. Zinc inhibited the enzyme system more than iron, manganese, or nickel. At 10––4 m, ferrous ion slightly stimulated the activity, but at 10––5 and 10––3 m, it was inhibitory. Manganese failed to stimulate the enzyme activity a

ISSN:0030-2414    

DOI:10.1159/000225144

出版商:S. Karger AG    

年代:1976

数据来源: Karger

摘要:

The action of free fatty acids on glycolytic enzymes was compared in normal and neoplastic tissues. Preincubation of tissue supernatant fractions with octanoate or laurate caused an inhibition of the activities of hexokinase and phosphofructokinase. An inhibition was also observed of lactate production with either glucose or glucose 6-phosphate as substrate. A similar degree of inhibition was observed for actions on normal liver and kidney, on the 7800 and 3924-A hepatomas and on the MK-3 renal cortical tumor. The possible relationship between the inhibition of glycolytic enzymes by fatty acids and anti-tumor activity previously observed with these compounds was noted.

ISSN:0030-2414    

DOI:10.1159/000225145

出版商:S. Karger AG    

年代:1976

数据来源: Karger

摘要:

The effect(s) of lack of dietary pyridoxine (PX) on the growth of Morris hepatoma no. 7288Ctc was studied. Buffalo strain female rats were fed a diet lacking PX. Pair-fed controls were fed the same diet with PX added. Animals were inoculated with no. 7288Ctc hepatoma cells at 21 days and were sacrificed 16 days later. Host livers and tumors were removed, weights recorded and the activity of tyrosine aminotransferase (TAT; L-tyrosine: 2-oxoglutarate aminotransferase, EC 2.6.1.5) was determined in both host liver and hepatoma. The average weight of 30 hepatomas grown in pair-fed control rats was 11.61 ± 1.5 g while the average weight of the same number of hepatomas grown in animals fed the PX free diet was 4.73 ± 0.7 g (P < 0.001). Further TAT specific activity levels were 39% and 32% higher in host livers and tumors from deficient animals, respectively. The results show that availability of dietary pyridoxine stimulates the growth of this hepatoma and, in addition, exercises a type of control over the expression of TAT activit

ISSN:0030-2414    

DOI:10.1159/000225146

出版商:S. Karger AG    

年代:1976

数据来源: Karger

摘要:

Cytoplasmic tyrosine transaminase (L-tyrosine: 2-oxoglutarate aminotransferase, EC 2.6.1.5) was partially purified from normal, host liver and three Morris hepatomas and subsequently resolved by electrophoresis on polyacrylamide gels. Enzyme activity was detected histochemically in situ on the gels. Seven enzymatically active forms were detected in normal liver. The presence of growing hepatomas altered significantly the expression of this enzyme. Only one, two and four activity peaks were detected in the host liver of animals with highly (most liver-like), well and poorly (least liver-like) differentiated hepatomas, respectively. Similarly, only one, four and six peaks were detected, respectively, in highly, well and poorly differentiated hepatomas.

ISSN:0030-2414    

DOI:10.1159/000225147

出版商:S. Karger AG    

年代:1976

数据来源: Karger

摘要:

The possibility that C’3 participates in tumor rejection was investigated in DBA/2 mice previously immunized against L1210 leukemia and in Swiss mice previously immunized against Ehrlich’s adenocarcinoma. In both the cases, animals treated with an appropriate dose of cobra venom factor to produce a C’3 depletion for some days after the tumor challenge, developed the neoplasia and had a mortality rate analogous to that of non-immunized animals. Studies on the peritoneal washing cells obtained at different times after the challenge revealed that in C’3 depleted immunized mice IgM are present on lymphocytes, macrophages and tumor cells, as in the immunized controls, but no contact between the cells and no macrophage phagocytosis were observed and the number of tumor cells increased progressively. These findings indicate that C’3 is critically involved in the rejection of the experimental tumors c

ISSN:0030-2414    

DOI:10.1159/000225148

出版商:S. Karger AG    

年代:1976

数据来源: Karger

摘要:

The growth of experimental tumors was found to involve an intensification of acetylation of sulphadimidine. Inhibition of carcinosarcoma Walker-256 by 88% and sarcoma-180 by 36% on treatment with 60 mg/kg body weight of hydrazine sulphate was followed by decreases in the rate of acetylation of 39.4 and 29.4%, respectively. When treatment failed to suppress tumor growth (sarcoma-45), acetylation level showed no decrease. The results point to a correlation between growth of tumors and their inhibition on the one hand and the level of acetylation on the other.

ISSN:0030-2414    

DOI:10.1159/000225149

出版商:S. Karger AG    

年代:1976

数据来源: Karger

摘要:

A carotenoid compound, crocetin, was used in two different types of tests involving animal tumors. These tests showed that crocetin both decreased the numbers of tumors as well as delaying onset.

ISSN:0030-2414    

DOI:10.1159/000225150

出版商:S. Karger AG    

年代:1976

数据来源: Karger

摘要:

A single oral carcinogenic (20 mg) dose of 7,12-dimethylbenz(a)anthracene (DMBA) significantly reduced the uterine nuclear uptake of estrogen-receptor complex when immature Sprague-Dawley rats were injected with 0.05 μg of tritiated estradiol-17β (E2) 24 hours after DMBA. Incubation experiments with whole uteri or with isolated uterine nuclei showed that DMBA in vitro does not act by reducing estrogen-receptor transformation or transport into nuclei. DMBA may act in vivo by stimulating hepatic degradation of injected estradiol-17β so that less active form of the steroid reaches target tissu

ISSN:0030-2414    

DOI:10.1159/000225151

出版商:S. Karger AG    

年代:1976

数据来源: Karger

摘要:

GP 48 989 causes regression of DMBA-induced mammary carcinomas of spayed (“hormone-independent”), non spayed (∼5% “hormone-dependent”) rats and of tumors which had become refractory to estradiol treatment. Since no binding to the cytoplasmic estradiol receptor after prolonged intramuscular treatment was found, the compound does not act as a classical anti

ISSN:0030-2414    

DOI:10.1159/000225152

出版商:S. Karger AG    

年代:1976

数据来源: Karger