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T Trenti

Publications and source records attributed to T Trenti.

29 records · Page 2Linked to original sources
PubMed1985

The effect of ferric iron complex on isolated rat liver mitochondria. I. Respiratory and electrochemical responses.

Addition of iron(III)-gluconate complex to isolated rat liver mitochondria resulted in an increased iron content of mitochondria. Iron was accumulated through a relatively fast process (maximal uptake in less than 2 min incubation) by an energy-independent mechanism. The in vitro iron overload of mitochondria was associated with enhancement in the oxygen consumption, which was due to the induction of lipoperoxidative processes catalyzed by iron. It was found that a concentration of iron as low as 0.1 mM elicits a consistent production of malondialdehyde in mitochondria. Concomitant with the induction of lipoperoxidation a progressive fall in the mitochondrial membrane potential was observed. The occurrence of energy-consuming processes as a consequence of iron addition, and particularly the enhancement of endogenous Ca2+ cycling across the membrane, was suggested as the cause of the membrane potential drop.

Animals↗
PubMed1985

The effect of ferric iron complex on isolated rat liver mitochondria. II. Ion movements.

It has been found that addition of iron(III)-gluconate complex to rat liver mitochondria disturbed the mitochondrial Ca2+ transport. Indirect evidence when the changes in the membrane potential during the transport of Ca2+ were followed, as well as direct evidence, when the fluxes of Ca2+ were monitored by a Ca2+-selective electrode, indicated that this iron complex induced an efflux of Ca2+ from liver mitochondria. The mechanisms by which iron induced Ca2+ release appeared to be linked to the induction of lipoperoxidation of mitochondrial membrane. The mitochondrial membrane, however, did not become irreversibly damaged under these conditions, as indicated by its complete repolarization. It was also shown that the induction by iron of lipoperoxidation brought about an efflux of K+ from mitochondria.

Animals↗
PubMed1985

The effect of ferric iron complex on Ca2+ transport in isolated rat liver mitochondria.

The in vitro effects of iron (III)-gluconate complex on the production of malondialdehyde and on the Ca2+ transport in isolated rat liver mitochondria were studied. A correlation between the concentration of iron added and the formation of malondialdehyde was found. The enhancement by iron of lipid peroxidative process in the mitochondrial membrane brought about the induction of Ca2+ release from mitochondria. Experimental evidence based on the membrane potential pattern of mitochondria pre-loaded with a low pulse of Ca2+ suggested that Ca2+ efflux was not due to a nonspecific increase in the inner membrane permeability, i.e. to a collapse of membrane potential, but rather to the activation of an apparently selective pathway for Ca2+ release.

Animals↗
PubMed1985

The role of pentachlorophenol in causing mitochondrial derangement in hexachlorobenzene induced experimental porphyria.

Hexachlorobenzene feeding to rats for 60 days to induce experimental porphyria resulted in partial and constant uncoupling of oxidative phosphorylation of liver mitochondria from the early phase (i.e. 20 days) of treatment. Direct experimental evidence has been presented that this uncoupling is completely due to the action of pentachlorophenol endogenously formed by metabolism of hexachlorobenzene. The complete restoration of membrane potential by albumin under these conditions indicates that no irreversible damage occurs in the mitochondrial membrane. No appreciable correlation between concentrations of pentachlorophenol and the degree of porphyria has been observed.

Animals↗
PubMed1984

Transmembrane potential of liver mitochondria from hexachlorobenzene-and iron-treated rats.

The respiratory parameters and the membrane potential of liver mitochondria from rats treated with either hexachlorobenzene, iron or hexachlorobenzene plus iron, to induce experimental porphyria, have been studied. Partial uncoupling of oxidative phosphorylation has been observed in mitochondria from hexachlorobenzene- and hexachlorobenzene plus iron-treated rats. Direct evidence has been presented that this uncoupling is due to the action of pentachlorophenol endogenously formed by metabolism of hexachlorobenzene. No irreversible damage of mitochondria membrane has been revealed under both these conditions. Normal oxidative phosphorylation has been found in mitochondria from rats treated with iron alone. In contrast, they presented an anomalous membrane potential, fully restored by oligomycin. A possible involvement of lipid peroxidation process, induced by iron, in causing these abnormalities has been suggested.

Animals↗
PubMed1984

Functional efficiency of mitochondrial membrane of rats with hepatic chronic iron overload.

The effect of in vivo hepatic iron overload, induced by two different amounts of iron, on the energy-transducing efficiency of the mitochondrial membrane has been examined. It has been found that when the epatic iron concentration is up to a threshold value mitochondria present an anomalous membrane potential. Addition of oligomycin fully restitutes it. A low content of intramitochondrial K+ is connected with this pathological condition. A relative lack of antioxidant capability is parallely exhibited by these mitochondria. A possible involvement of lipid peroxidation process in vivo in causing the membrane potential drop and the net efflux of intramitochondrial K+ is suggested.

Animals↗
PubMed1984

Structural and functional properties of rat liver mitochondria in hexachlorobenzene induced experimental porphyria.

A possible link between changes in iron and porphyrin content in liver mitochondria, from rats treated with either hexachlorobenzene, iron, or hexachlorobenzene plus iron, as a function of treatment time and their structural-functional properties, has been investigated. Normal oxidative phosphorylation in mitochondria from rats treated with iron has been shown. By contrast a significant and constant uncoupling of the phosphorylative process, fully reversed by albumin, in mitochondria from rats treated with hexachlorobenzene and hexachlorobenzene plus iron has been presented. A possible involvement of pentachlorophenol in causing these abnormalities has been proposed.

Animals↗
PubMed1984

Coproporphyrin excretion in healthy newborn babies.

The urinary and fecal coproporphyrins (CP) undergo significant changes in cholestatic diseases of both adults and infants and their determination may provide a diagnostic tool. Little is known about CP excretion in the first days of life. The authors have studied the daily urinary and fecal excretion of CP as well as the I and III isomer distribution in 10 healthy newborn babies from 1 to 10 days old. CP were determined by the solvent partition method and the isomer distribution by thin-layer chromatographic technique. Preliminary studies on urinary porphyrin pattern were performed using a personal high-performance liquid chromatographic method. CP excretion was almost 10 times higher on the 1st day than on the 10th, when expressed by adult standards. The isomer I accounted for almost 80% of the total amount on the first days, whereas at the end of the study, both the CP total amount and isomer distribution overlapped the infant and adult pattern. The authors propose a personal interpretation based on a possible transient enzymatic defect in the metabolic chain of heme synthesis.

Chromatography, High Pressure Liquid↗
PubMedDate not supplied

Fructosamine and glycated hemoglobin as indices of glycemic control in patients with liver cirrhosis.

Glucose intolerance often occurs in liver cirrhosis; therefore a long-term control of plasma glucose levels appears to be important. For this purpose glycated hemoglobin A (HbA1c) determination is proposed as a suitable method, while no data are available on fructosamine test. In 98 cirrhotic patients serum fructosamine and HbA1c levels were compared with those of normal controls and among cirrhotic patients grouped in non glucose-intolerant and with non insulin-dependent (NIDDM) or insulin-dependent diabetes mellitus (IDDM). The mean HbA1c values of cirrhotic patients with normal glycemic control were significantly lower than normal, and only a few IDDM and NIDDM cirrhotic patients showed high values of HbA1c, indicating that HbA1c is often underestimated in these patients. On the contrary, serum fructosamine levels were on the average higher than normal in nondiabetic patients, but they were significantly higher in IDDM and NIDDM patients than in nondiabetics, and the 72% of NIDDM and 85% of IDDM patients had fructosamine levels higher than the upper normal value. In conclusion, in diabetic patients with liver cirrhosis fructosamine seems to be a more suitable test than HbA1c for monitoring blood glucose levels.

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