Phosphorylation and redox states in ischemic liver

Gaja, G.; Ferrero, Maria Elena; Piccoletti, Roberta; Bernelli‐Zazzera, Aldo

doi:10.1016/0014-4800(73)90083-x

Cited by 46 publications

(21 citation statements)

References 28 publications

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“…Gaja et al [6] reported that the upper limit of rever sal is 60 min. The effects of ischemia on liver mitochondrial function has been reported by several workers, with evidence to indicate that mitochondrial function exclusively de teriorates along with the time of ischemia [6,27], On the other hand, previous studies have demonstrated an enhanced mitochon drial function in liver tissue in partial hepatectomy or portal vein ligation in which model changes in blood flow through the liver always occur [18,20], The present ex periment is aimed at obtaining more infor mation on the effects of partial hepatic vas cular occlusion and subsequent reflow on mitochondrial function and energy metabo lism in the rat liver. Both the reversal of mitochondrial dysfunction of the ischemic lobe and the enhancement of mitochondrial function of the nonischemic lobe will be shown and discussed.…”

Section: Introductionmentioning

confidence: 99%

“…The liver of mam mals can tolerate up to 30-60 min of isch emia and still resume normal functioning after recirculation of oxygenated blood [3,4,6,9]. Different species have different time limits for the reversibility of impaired he patic function due to their dissimilar vascu lar anatomy of the liver [7], Moreover, even within the same species, there is no absolute point beyond which cellular changes become irreversible because of differences in strain, diet and biological factors [4,21,32].…”

Section: Introductionmentioning

confidence: 99%

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Effects of Partial Ischemia and Reflow on Mitochondrial Metabolism in Rat Liver

et al. 1988

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To clarify the effects of partial ischemia and reflow on the mitochondrial metabolism of the rat liver, the afferent vessels supplying the left lateral and left half of medial lobes were occluded and then reperfused after given time periods of ischemia (30, 60, 90 and 120 min, groups A, B, C and D, respectively). Samplings were taken at 0, 10 and 60 min after reperfusion. The energy charge levels of ischemic lobes decreased rapidly from 0.85 ± 0.01 in the sham group to 0.38 ± 0.11, 0.35 ± 0.07 and 0.34 ± 0.06 in groups B, C and D, respectively. The phosphorylative activities of mitochondria isolated from ischemic lobes decreased gradually along with the time of ischemia. The reversal of mitochondrial function and energy charge levels following reperfusion was noted in groups A and B. In nonischemic lobes, the phosphorylation rate (nmol ATP/mg/min) increased from 90 ± 6 in sham group to 125 ± 12 and 130 ± 9; 131 ± 5 and 130 ± 6; 123 ± 6 and 122 ± 17, and 138 ± 6 and 138 ± 13 at 10 and 60 min after reflow in groups A, B, C and D, respectively (p < 0.05). The energy charge level of nonischemic lobes decreased from 0.85 ± 0.01 of sham group to 0.80 ± 0.03 in group D (p < 0.05). From these results, it is concluded that the transitional zone for the reversal of mitochondrial function and energy metabolism following prolonged liver ischemia appears at around 60 min. It is suggested that there exist some mechanism(s) which lead to an enhancement of mitochondrial function in nonischemic lobe after reflow.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of Partial Ischemia and Reflow on Mitochondrial Metabolism in Rat Liver

et al. 1988

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“…There are many reports that show ischemia to cause functional and structural damage to liver cells [2][3][4][5][6]. Such damage can be caused by the accumulation of LPO that partly results from decreased SOD activity as a consequence of membrane disorders following cerebral hemorrhage [7].…”

Section: Discussionmentioning

confidence: 99%

“…It is well known that ischemia causes functional and structural damage to liver cells [2][3][4][5][6]. It is also known that the accumulation of LPO seen following cerebral hemorrhage partly results from decreased activity of superoxide dismutase (SOD) as a consequence of membrane disorder [7].…”

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Leakage of monoamine oxidase from rat liver after hepatic ischemia or administration of the hepatotoxin allyl formate.

Obata

Yamanaka

1989

J. Clin. Biochem. Nutr.

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“…From the analysis of the results obtained in various laboratories (Williamson et al, 1967;Brosnan et al, 1970;Gaja et al, 1973;Sox & Hoagland, 1966;Pilkis & Korner, 1971;Smuckler & Trump, 1968;Ragnotti et al, 1970;Cajone et al, 1971;Nolan & Hoagland, 1971) it appears that an increased reduction of the cytoplasm is constantly accompanied by polyribosomal disaggregation and by a decreased rate of protein biosynthesis and that these alterations are promptly reversed on normalization of the redox state. Further, preliminary experiments performed in our laboratory have demonstrated that, in agreement with the findings of Murthy (1966), the addition of NADPH or NADH to a cell-free system inhibits protein synthesis in a concentrationdependent fashion.…”

Section: Vol 146mentioning

confidence: 99%

The effect of phenobarbitone on protein synthesis by liver polyribosomes in fed and starved rats

Ragnotti

Aletti

1975

Biochemical Journal

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1. The effect of phenobarbitone on the rate of protein synthesis and on the sedimentation patterns of various liver subcellular fractions containing ribosomes was studied in rats. 2. Phenobarbitone treatment increased the incorporation of [14C]leucine into protein by all preparations, provided they had not been subjected to preliminary treatment with Sephadex G-25. The phenobarbitone-induced effect on incorporation was associated with a gain in liver weight and a higher degree of polyribosomal aggregation. 3. Preparations that were treated with Sephadex G-25 incorporated more radioactivity into protein, but did not show the response to phenobarbitone treatment. 4. When the influence of starvation and phenobarbitone was studied separately on membrane-bound and membrane-free polyribosomes, it was shown that whereas both classes of polyribosomes were affected by starvation, apparently only the former class was susceptible to phenobarbitone stimulation of protein synthesis. 5. The decreased capacity for protein synthesis of polyribosomes from starved rats was independent of their association with the membranes of the endoplasmic reticulum, but resulted from polyribosomal disaggregation, from an intrinsic defect of the polyribosomes themselves and from changes in composition of the cell sap. 6. The results are discussed in relation to the problem ofthe control ofprotein biosynthesis and of the functional separation of membrane-bound and membrane-free polyribosomes.

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Phosphorylation and redox states in ischemic liver

Cited by 46 publications

References 28 publications

Effects of Partial Ischemia and Reflow on Mitochondrial Metabolism in Rat Liver

Effects of Partial Ischemia and Reflow on Mitochondrial Metabolism in Rat Liver

Leakage of monoamine oxidase from rat liver after hepatic ischemia or administration of the hepatotoxin allyl formate.

The effect of phenobarbitone on protein synthesis by liver polyribosomes in fed and starved rats

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