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Biomedical subjects

C G Fraga

Publications and source records attributed to C G Fraga.

45 records · Page 3Linked to original sources
PubMed1988

Lipid peroxidation measured as thiobarbituric acid-reactive substances in tissue slices: characterization and comparison with homogenates and microsomes.

Liver slices were used to measure lipid peroxidation induced by bromotrichloromethane, tert-butyl hydroperoxide (t-BOOH), or ferrous iron. The responses of liver homogenates and microsomes to oxidative conditions were compared with the response of tissue slices. Lipid peroxidation was evaluated by the production of thiobarbituric acid-reactive substances (TBARS). As was observed in homogenates and microsomes, TBARS production by liver slices depended upon the amount of tissue, the incubation time, inducer, the amount of inducer, and the presence of antioxidant. Control liver slices incubated at 37 degrees C for 2 h produced 19 nmol of TBARS per g of liver. When slices were incubated in the presence of 1 mM BrCCl3, 1 mM t-BOOH, or 50 microM ferrous iron, TBARS production increased 4.6-, 8.2-, or 6.7-fold over the control value, respectively. Comparable induction of TBARS by liver homogenates and microsomes was observed when these preparations were incubated with the same inducers. Addition of 5 microM butylated hydroxytoluene (BHT) prevented the induction of TBARS by 50 microM ferrous iron by liver slices. The results indicate the usefulness of tissue slices to measure lipid peroxidation. The usefulness of tissue slices is emphasized when a number of compounds or tissues are studied and tissue integrity is desired as in toxicological, pharmacological, and nutritional studies where reduced numbers of experimental animals is a relevant issue.

Animals↗
PubMed1987

Flavonoids as antioxidants evaluated by in vitro and in situ liver chemiluminescence.

Administration of eriodyctiol and (+)-catechin (10 mg/100 g of body weight) to mice inhibited the enhancement of in situ liver chemiluminescence produced by CCl4 (0.5 ml/100 g) by 32 and 38% respectively. 3,4-Dicaffeoylquinic acid was less effective (13%), and cynarin had no effect. Previously, these compounds and other polyphenols were assayed as in vitro antioxidants by their abilities to inhibit the tert-butyl hydroperoxide (t-BOOH)-initiated chemiluminescence of mouse liver homogenates, and the IC50 (microM) values were as follows: (+)-catechin, 3; eriodyctiol, 9; myricetin and 4,2',4'-trihydroxy-6'-metoxychalcone, 15; 3,4-dicaffeoylquinic acid, 20; isochlorogenic acid, 30; caffeic acid, 5,6,3'-trihydroxy-7,4'-dimethoxyflavone and cynarin, 50; chlorogenic acid and apigenin, 150; quercetin, pedalitin, sylimarin and quercetin-3-methyl ester, 200; 7,4'-dihydroxy-5-methoxyflavonone and kaempferol-3,7-dirhamnoside, 500; quercitrin, 900; and galangin-3-methyl ether, genkwanin, hesperidin, ombuoside, phloridzin, quinic acid, rhoifolin, rutin and sophoricoside, greater than 1 mM. The in vitro and in vivo effects of these flavonoids and polyphenols may be related to their antioxidant abilities, making them promising substances to be investigated as water-soluble protectors against lipid peroxidation and other free radical-mediated cell injury.

Animals↗
PubMed1987

Effect of vitamin E- and selenium-deficiency on rat liver chemiluminescence.

The role of vitamin E and selenium as protective agents against oxidative stress was evaluated by measuring liver chemiluminescence in situ. Weanling rats fed a vitamin E- and selenium-deficient diet showed liver chemiluminescence that was increased 60 and 100% over control values at 16 and 18 days respectively after weaning. At day 21, the double deficiency led to hepatic necrosis, as observed by optical and electron microscopy, and increased serum levels of lactate dehydrogenase and alanine aminotransferase. Single deficiencies, in either vitamin E or selenium, did not produce liver necrosis but increased liver chemiluminescence. Vitamin E deficiency led to a 23 and 50% increase in liver emission at days 18 and 20 respectively; selenium deficiency produced a 64% increase at day 16. The activity of liver selenium-glutathione peroxidase diminished to 13% of the control value in the rats fed doubly deficient and selenium-deficient diets. Activities of superoxide dismutase, catalase and non-selenium-glutathione peroxidase were not modified by the different diets. These results suggest that oxy-radical generation may play a major role in hepatic necrosis in vitamin E- and selenium-deficiency.

Animals↗
PubMed1987

Halogenated compounds as inducers of lipid peroxidation in tissue slices.

Twenty-seven halogenated compounds were screened as potential inducers of lipid peroxidation in rat liver, kidney, spleen, and testes slices. In addition to the known lipid peroxidation inducers--carbon tetrachloride and bromotrichloromethane--the novel compounds carbon tetrabromide, p-bromobenzyl bromide, and benzyl bromide increased lipid peroxidation in each of the tissues studied. Lipid peroxidation was measured by release of thiobarbituric acid-reactive substances (TBARS) from the tissue slices. The amount of TBARS released from liver slices incubated with bromotrichloromethane, carbon tetrabromide, dichloromethane, bromobenzene, chloroform, bromoform, benzyl chloride, bromochloromethane, and carbon tetrabromide correlated with the lethality of these compounds as evaluated by their oral LD50 in rats. The lethality of a number of the compounds tested did not correlate with their capacity to induce lipid peroxidation.

Animals↗
PubMed1985

Increased liver chemiluminescence in tumor-bearing mice.

Spontaneous mouse liver chemiluminescence (109 +/- 6 cps/cm2) was increased in the early phase after tumor implantation in a distant position with respect to the liver. A 39% increased liver chemiluminescence was observed after 5 days of the injection of Ehrlich ascites tumor cells into the peritoneal cavity, and a 64% and a 46% increased liver chemiluminescence were measured after 8 and 14 days of the implantation of a fibrosarcoma and of an adenocarcinoma, respectively, in the leg. At the time of maximal stimulation of in vivo liver chemiluminescence by the distant tumors, cytosolic superoxide dismutase, catalase, and glutathione peroxidase activities were decreased by 18%, 38%, and 26% in the liver of mice bearing Ehrlich ascites tumors. The same three enzymatic activities were decreased by 21%, 19%, and 54% respectively, in the liver of fibrosarcoma-bearing mice. Total liver glutathione was decreased by 18% to 22% in the tumor-bearing animals. Hydroperoxide-initiated chemiluminescence was increased in the homogenates (105% and 45%) and mitochondria (64% and 34%) from the liver of mice bearing Ehrlich ascites tumors and fibrosarcomas, respectively, at the time of maximal in situ liver chemiluminescence. The hydroperoxide-initiated chemiluminescence of liver microsomes was decreased by 46% to 36% in the tumor-bearing animals at the same time. It is concluded that the liver of tumor-bearing animals is subjected, during the early phase after tumor implantation, to an oxidative stress with increased steady-state levels of peroxyl radicals, which are essentially responsible for the increased photoemission observed in vivo.

Adenocarcinoma↗
PubMed1984

Increased carbon tetrachloride-stimulated chemiluminescence in the in situ liver of barbital-treated mice.

Mice treated with barbital (0.1% in the drinking water) during 15 days showed a 63% increased endoplasmic reticulum mass. The carbon tetrachloride-stimulated chemiluminescence of the in situ liver was 51% increased after barbital treatment. Hydroperoxide-stimulated chemiluminescence of liver homogenates and microsomal suspensions were increased by 140 and 92%, respectively, in the barbital-treated mice. Spontaneous liver chemiluminescence (109 cps/cm2) was found unchanged after barbital treatment. Superoxide dismutase, catalase and glutathione peroxidase activities were 109, 61 and 103%, respectively, increased after barbital treatment. The results are consistent with a primary role of cytochrome P 450 in the biotransformation of CCl4, which initiates a radical chain reaction leading to the production of powerful oxidizing species. Apparently, superoxide dismutase, catalase and glutathione peroxidase are synthetized in a coincident manner with respect to cytochrome P 450.

Animals↗
PubMed1983

Increased chemiluminescence and superoxide production in the liver of chronically ethanol-treated rats.

Rats fed ethanol (1.74 +/- 0.12 g/day/100 g body wt for 12 weeks) showed a 45% increased microsomal production of O-2 (2.23 +/- 0.14 nmol/min/mg protein) and a 28% increased content of endoplasmic reticulum protein (26.8 +/- 1.4 mg/g liver). This could lead, at substrate saturation, to a 86% increased cytosolic production of O-2 which is not compensated by cytosolic superoxide dismutase levels that remain normal. It is claimed that this unbalance between O-2 production and superoxide dismutase leads to a peroxidative stress in agreement with the 54% increased spontaneous liver chemiluminescence (37 +/- 2 cps/cm2) measured in the ethanol-treated rats. Hydroperoxide-induced chemiluminescence was 57, 43, and 28% higher, respectively, in homogenates, mitochondria, and microsomes isolated from ethanol-treated rats as compared with controls. Vitamins E and A were more effective inhibitors of the hydroperoxide-stimulated chemiluminescence in the liver homogenates from ethanol-treated rats as compared with the effect on the homogenates from control animals. The results are consistent with a peroxidative stress in chronic alcoholism leading to increased lipoperoxidation and decreased levels of antioxidants.

Animals↗