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1.
Annette Graham 《Free radical research》1998,28(6):611-621
Compelling evidence suggests that low-density lipoprotein (LDL) is oxidized by cells within the arterial intima and that, once oxidized, it is profoundly atherogenic. The precise mechanism(s) by which cells promote the oxidation of LDL in vivo are not known; in vitro, however, oxidation of LDL can be enhanced by a number of differing mechanisms, including reaction with free and protein-bound metal ions, thiols, reactive oxygen species, lipoxygenase, myeloperoxidase and peroxynitrite. This review is concerned with the mechanisms by which cells enhance the oxidation of LDL in the presence of transition metals; in particular, the regulation, pro- and anti-oxidant consequences, and mechanism of action of cellular thiol production are examined, and contrasted with thiol-independent oxidation of LDL in the presence of transition metals. 相似文献
2.
《Fungal biology》2020,124(2):83-90
Latterly, the upsurge in use of antifungal drugs has brought about the emergence of several drug-resistance strains, making it skeptical to continue relying on current therapeutic regime. In the necessity of resistance-free antifungal agent, flavonoids presented possibilities of replacing existing drugs, displaying antifungal activity against pathogenic fungi. Among them, quercetin, one of the most representative flavonoids, exhibited antifungal activity against Candida albicans. To inspect the further understanding regarding quercetin, the antifungal mode of action of quercetin was investigated. In the initial step, the apoptosis was monitored after quercetin treatment. Moreover, intracellular levels of Mg2+ was assessed and was determined that Mg2+ increase occurred under the influence of quercetin. In addition, several features of mitochondrial dysfunction were monitored. Mitochondrial dysfunction triggers decrease in mitochondrial redox levels and leads to disruption in mitochondrial antioxidant system. Increased intracellular ROS and decreased intracellular redox levels were also displayed, indicating the occurrence of overall disruption in antioxidant systems. Sequentially, DNA fragmentation was observed and this DNA damage in turn induces apoptosis. In analyses, hexaamminecobalt(III) chloride (Cohex) was applied to inhibit Mg2+ transport between cytosol and mitochondria. Cohex attenuated the effects induced by quercetin, which demonstrates that the presence of Mg2+ is essential in quercetin-induced apoptosis. 相似文献
3.
4.
Ronald J.A. Wanders Carlo Van Roermund Cor Lof Alfred J. Meijer 《Analytical biochemistry》1983,129(1):80-87
A simple fluorimetric assay for the determination of carbamoyl phosphate in tissue extracts is described. In the assay, production of ATP from carbamoyl phosphate and ADP by carbamate kinase is coupled to the formation of NADPH, using glucose, hexokinase, NADP+, and glucose-6-phosphate dehydrogenase. Production of NADPH in this system proved to be equal to the amount of carbamoyl phosphate present. 相似文献
5.
6.
The rapid increase in protein synthesis that occurs on addition of insulin (1 mU/ml) to stepped-down 3T3 cells was blocked by pre-incubation of the cells with pertussis toxin. Cholera toxin on the other hand stimulated protein synthesis and this effect was insensitive to actinomycin D and inhibited by pro-treatment of the cells with phorbol dibutyrate to deplete cell protein kinase C. Insulin was found to cause a rapid and transient increase in diacylglycerol (DAG) synthesis. The insulin-induced increase in diacylglycerol was blocked by pertussis toxin. Exogenous DAG (10 M) stimulated protein synthesis within 1 hour. The results suggest that insuIin stimulates ribosomal activity through a signal mechanism that involves a G-protein mediated activation of phospholipase C to increase DAG levels. 相似文献
7.
The activity of the enzymes 5'-nucleotidase (EC 3.1.3.5), adenosine nucleosidase (EC 3.2.2.7), adenine phosphoribosyl transferase (EC 2.4.2.7) and acid phosphatase (EC 3.1.3.2) was determined in sections of tomato plant ( Lycopersicon esculentum Mill. cv. Bellina). The distribution of the enzymes changed markedly during development and a role for these enzymes in cytokinin metabolism is suggested. 相似文献
8.
The mechanism of hypercholesterolemia effect of Cu2+ deficiency was studied in rats. There was increased activity of hepatic hydroxymethylglutaryl-coenzyme A reductase and increased
incorporation of labelled acetate into free cholesterol of liver in the Cu2+ deficient rats. Incorporation of label into ester cholesterol was however decreased in the liver. Concentration of bile acids
in the liver was not significantly altered. Increase in the incorporation of labelled acetate into serum cholesterol and increase
in the concentration of cholesterol and apo B in the low density lipoproteins + very low density lipoproteins fractions were
observed. Activity of lipoprotein lipase of the extrahepatic tissues decreased in the Cu2+ deficient rats. 相似文献
9.
Three compounds capsaicin, curcumin and ferulic acid showing hypolipidemic activity have been tested in adult Wistar rats
fed high fat diets. Capsaicin (0.20 mg%) fed to female rats along with a 30% saturated fat diet lowered the rate of weight
gain, liver and serum triglycerides. In male rats it lowered only the liver and serum total and very low density and low density
lipoprotein triglycerides whether fed continuously for 13 or 8 weeks after interchanging the control and test diets from the
5th week onwards. Capsaicin fed to female rats in 30% mixed fat diet increased the rate of weight gain, lowered liver and
serum triglycerides, lowered adipose tissue lipoprotein lipase, elevated the hormone sensitive lipase and serum free fatty
acids. Capsaicin in 30% saturated fat diet lowered both the enzyme activities to a much lesser extent. Curcumin and ferulic
acid (both at 25 mg%) in 30% saturated fat diet tended to lower the rate of weight gain, liver total lipids and serum triglycerides.
It is of significance that a common dietary compound ‘capsaicin’ in the range of human intake triggers lipid lowering action
in rats fed high fat diets.
This paper was presented at the 55th Annual Meeting of the Society of Biological Chemists (India) held at Trivandrum during
December 15–17th, 1986. 相似文献
10.
Genetic analysis of murine strains C57BL/6J and C3H/HeJ to confirm the map position ofAth-1, a gene determining atherosclerosis susceptibility 总被引:4,自引:0,他引:4
Beverly Paigen Deborah Albee Patricia A. Holmes Diane Mitchell 《Biochemical genetics》1987,25(7-8):501-511
Previous results suggested that strains C57BL/6J and C3H/HeJ differed in a single gene for atherosclerosis susceptibility, calledAth-1. Based on data from recombinant inbred strainsAth-1 was tentatively assigned to chromosome 1 linked toAlp-2. In this report, a cross between C57BL/6 and C3H/HeJ was carried out in order to test whether the tentative map position was correct. Parental strains and F1 and F2 progeny were examined. Susceptible alleles ofAth-1, found in C57BL/6, are associated with relatively low levels of high-density lipoprotein (HDL)-cholesterol in animals fed an atherogenic diet; resistant alleles ofAth-1 are associated with relatively high levels of HDL-cholesterol. F1 progeny have HDL levels that are intermediate between these of the two parental strains. Among the F2 progeny,Alp-2 andAth-1 cosegregated, providing confirmatory evidence thatAth-1 is linked toAlp-2 on chromosome 1. Three mice recombinant forAlp-2 andAth-1 were found among the 60 chromosomes tested, giving an estimated map distance between these two genes of 5.0±2.8 (SE) cM. The phenotypic characteristics ofAth-1 resemble a genetic trait in humans, hyperalphalipoproteinemia, which is characterized by elevated levels of HDL-cholesterol, reduced risk of heart disease, and increased longevity.This work was supported by Grant HL-32087 from the Heart, Lung, and Blood Institute, National Institutes of Health, Grant 1858 from the Council for Tobacco Research, Grant 86-1387 from the American Heart Association with funds contributed in part by the Alameda, Orange, and Santa Barbara County Chapters, and Grants 85-N132A and 85-N136A from the California Affiliate of the American Heart Association. 相似文献