Biomedical subjects

S Banni

Publications and source records attributed to S Banni.

23 records · Page 2Linked to original sources

PubMed1989

Free radicals and lipid peroxidation in liver of rats kept on a diet devoid of choline.

Rodents kept on a choline devoid (CD) diet up to 14 months develop hepatic lesions progressing through two broad stages. The first is characterized by severe steatosis and increase in cell turnover, the second by a gradual clearance of the deposited fat and fibrosis. Hepatocellular carcinomas eventually arise in rats fed for over 12 months, even though the animals aer not exposed to chemical carcinogens. It has been suggested that the diet may trigger generated thereby may be responsible for initiation of liver cancer and promotion. The radicals would lead to DNA damage, and the altered DNA in a proliferating liver would result in initiation of the carcinogenic process. In this communication we present evidence that the diet used in the above studies contained stable fatty acid isomers with conjugated dienes, which are absorbed and deposited in rat liver. This finding cast doubts on whether a CD diet does indeed cause a peroxidation of cellular membrane lipids. Electron spin resonance (ESR) spectroscopy was also used to investigate whether any abnormal pattern of free radicals exists in the liver of rats fed a CD diet. No significant differences were noted in ESR spectra of either transition metal-centered signals, or organic free radicals.

Animals↗

PubMed1987

Free-radical metabolism of carbon tetrachloride in rat liver mitochondria. A study of the mechanism of activation.

Alterations in liver mitochondria as consequence of rat poisoning with carbon tetrachloride (CCl4) have been reported over many years, but the mechanisms responsible for causing such damage are still largely unknown. Isolated rat liver mitochondria incubated under hypoxic conditions with succinate and ADP were found able to activate CCl4 to a free-radical species identified as trichloromethyl free radical (CCl3) by e.s.r. spectroscopy coupled with the spin-trapping technique. The incubation of mitochondria in air decreased free-radical production, indicating that a reductive reaction was involved in the activation of CCl4. However, in contrast with liver microsomes (microsomal fractions), mitochondria did not require the presence of NADPH, and the process was not significantly influenced by inhibitors of cytochrome P-450. The addition of inhibitors of the respiratory chain such as antimycin A and KCN decreased free-radical formation by only 30%, whereas rotenone displayed a greater effect (approx. 84% inhibition), but only when preincubated for 15 min with mitochondria not supplemented with succinate. These findings suggest that the mitochondrial electron-transport chain is responsible for the activation of CCl4. A conjugated-diene band was observed in the lipids extracted from mitochondria incubated with CCl4 under anaerobic conditions, indicating that stimulation of lipid peroxidation was occurring as a result of the formation of free-radical species.

Animals↗

PubMed1987

MPTP fails to induce lipid peroxidation in vivo.

It has been speculated that the conversion of MPTP to MPP+ destroys dopaminergic neurons by promoting the generation of hydroxyl radicals and causes lipid peroxidation. The results obtained in the present work indicate that the primary products of lipid peroxidation are not detectable in MPTP treated animals and thus other mechanisms besides lipid peroxidation should be considered to explain the cytotoxicity of this neurotoxin.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed1987

NMR spin-lattice relaxation times of intracellular Na-23 on rat livers and related lipid peroxidation following CCl4 intoxication.

Liver tissues were isolated from rats acutely intoxicated with carbon tetrachloride, and Na-23 NMR signals were analyzed to investigate the T1 relaxation times of intracellular sodium ions under pathological conditions in presence of the paramagnetic shift reagent (dysprosium tripolyphosphate). We studied the significant increase of T1 found in CCl4 treated rats with respect to controls, which was elsewhere demonstrated as being independent of cell necrosis. Evidence is given that neither fat accumulation nor proliferative processes affect the observed T1 lengthening. When T1 relaxation times were measured in the liver of vitamin E treated rats subsequently intoxicated with carbon tetrachloride, a significative shortening of T1 with respect to CCl4-intoxicated rats was observed. These results were discussed in terms of the antioxidant action exerted by vitamin E, taking into account that peroxidation of microsomal lipids is the key factor in the process of carbon tetrachloride induced liver injury. Furthermore, the observed T1 changes were discussed in terms of the interactions of Na+ with cell membranes and/or the occurrence of viscosity changes.

Carbon Tetrachloride Poisoning↗

PubMedDate not supplied

Modulation of lipid metabolism and vitamin A by conjugated linoleic acid.

The term conjugated linoleic acid (CLA) refers to a collection of positional and geometrical isomers of octadeca- dienoic acid with conjugated double bonds. CLA has been shown to possess several beneficial activities in different experimental models, however, out of 28 isomers only two, c9, t11 and t10, c12 have been thus far demonstrated to be biologically active. The discovery that it can be elongated and desaturated as a regular fatty acid in human and animal tissues brought a new possibility that its activity may be related to its properties as a peculiar unsaturated fatty acid. In fact, CLA is able to be incorporated in lipid classes as oleic acid, accumulating in those tissues rich in neutral lipids; to be metabolized as linoleic acid and so influencing linoleic acid desaturation and elongation; and to be beta oxidized in peroxisomes which may account for, through activation of PPARs, its ability to increase free retinol levels and influence gene expression. These activities are amplified where CLA accumulates more such as mammary and adipose tissues and may explain its peculiar beneficial properties, at relative low dietary concentrations, in these tissues. Furthermore, it has been demonstrated that CLA can be endogenously formed by delta 9 desaturation of vaccenic acid (t11 18:1) thus forming the isomer c9, t11. Either endogenously formed or through dietary intake, CLA showed to be metabolized in the same way and to exert the same biological properties. We may conclude that a regular intake of CLA, or/and vaccenic acid as its precursor, should work as an excellent preventive agent by modulating lipid metabolism in target tissues thus conferring protection against the attack of insults of different type.

Adipose Tissue↗