Heterogeneity of rat liver mitochondrial fractions and the effect of tri-iodothyronine on their protein turnover

Katyare, Surendra S.; Fatterpaker, P.; Sreenivasan, A.

doi:10.1042/bj1180111

Cited by 56 publications

(28 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This may perhaps correlate with an increased content of cytochrome c + cl in mitochondria from this group of animals ( Table 5). The regulatory role of cytochrome c in succinate oxidation has previously been demonstrated by us (Katyare et al, 1970). Interestingly, paracetamol-induced lesions could be seen even in the subtoxic group in terms of impaired glutamate and succinate dehydrogenase activities (Table 4).…”

Section: Discussionmentioning

confidence: 59%

See 1 more Smart Citation

Impaired mitochondrial oxidative energy metabolism following paracetamol‐induced hepatotoxicity in the rat

Katyare

Satav

1989

British J Pharmacology

View full text Add to dashboard Cite

1 Effects of paracetamol treatment in vivo at subtoxic (375mgkg-' body weight) and toxic (750 mg kg-1 body weight) doses on energy metabolism in rat liver mitochondria were examined. 2 Paracetamol treatment resulted in a significant loss in body weights without affecting the liver protein contents. Toxic doses, however, resulted in 21% decrease in the yield of mitochondrial proteins.3 Subtoxic doses of paracetamol did not, in general, affect the respiratory parameters in the liver mitochondria except in the case of succinate where both the state 3 respiration and the ADPphosphorylation rates increased by 28%. 4 Toxic doses of paracetamol caused 25 to 47% decrease in the state 3 respiration rates depending on the substrate used. ADP/O ratios also decreased significantly with pyruvate + malate and succinate as the substrates. Consequently, ADP-phosphorylation was impaired significantly from 20 to 63%. 5 Subtoxic doses of paracetamol resulted in increased contents of cytochrome c + cl while the toxic doses caused lowering of the cytochromes aa3 and b contents. 6 Glutamate and succinate dehydrogenase activities decreased in both the experimental groups while Mg2 +-ATPase activity was impaired only after toxic dose-treatment. 7 The results show that toxic doses of paracetamol result in impaired energy coupling in the liver mitochondria. Effects of subtoxic doses were also demonstrable in terms of impaired dehydrogenases activities.

show abstract

Section: Discussionmentioning

confidence: 59%

“…This activity was not stimulated by Mg2+ alone but could be fully evoked by DNP or DNP + Mg2", thus emphasizing the intactness of the mitochondrial membranes (Katyare et al, 1970). This was also reflected in terms of high ratio of DNP/Mg2+ ATPase activities (Table 6).…”

Section: Resultsmentioning

confidence: 73%

Impaired mitochondrial oxidative energy metabolism following paracetamol‐induced hepatotoxicity in the rat

Katyare

Satav

1989

British J Pharmacology

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 75%

“…The lack of changes in the M 10 proteins could appear surprising since an increase of lightmitochondrial proteins 48 h after single T 3 injection has been found [40]. On the other hand, the finding that mitochondrial fraction obtained at 10,000 g has a shorter half-life than mitochondria obtained at 6,500 g [40], indicates that the light fraction rapidly changes into heavier fractions. It is, therefore, possible that the light-mitochondrial proteins, which increase after acute treatment, undergo a reduction after prolonged treatment, owing to the T 3 -induced increase in synthetic ability of light fraction [40], which should turn more quickly into the M 3 fraction.…”

Section: Discussionmentioning

confidence: 75%

Antioxidant-Sensitive Triiodothyronine Effects on Characteristics of Rat Liver Mitochondrial Population

Venditti

Magistro

Masullo

et al. 1999

Cell Physiol Biochem

View full text Add to dashboard Cite

Whole mitochondrial population and three mitochondrial fractions were resolved by differential centrifugation from liver homogenates from euthyroid, hyperthyroid (ten daily i.p. injections of triiodothyronine (T₃), 10 μg/100 g body weight) and hyperthyroid vitamin E-treated (ten daily i.m. vitamin E injections, 20 mg/100 g body weight) rats. Homogenates and mitochondrial preparations were examined for their protein content, oxidative capacity, lipid peroxidation, antioxidant status, and susceptibility to oxidative stress. In all groups, antioxidant level was smaller and oxidative capacity, lipid peroxidation, and susceptibility to oxidants were greater in the heavy mitochondrial fraction. T₃ treatment was associated with increased oxidative capacity, lipid peroxidation, and susceptibility to oxidative stress, and decreased antioxidant levels in all preparations. It was also associated with increased mitochondrial protein content of homogenate and altered quantitative presence of the mitochondrial fractions. The vitamin E effects on the T₃-induced changes were different for the different parameters. Vitamin E did not modify the mitochondrial protein content in liver and oxidative capacity of the various preparations, reduced the changes in both susceptibility to oxidants and contribution of each fraction to the whole mitochondrial population, and reinstated euthyroid values for antioxidant capacity and lipid peroxidation. The incomplete recovery of euthyroid resistance to oxidants in vitamin E-treated rats is due to the vitamin inability to reinstate the levels of both antioxidants and hemoproteins, on which such a resistance depends. The vitamin E effect on the composition of the mitochondrial population is more difficult to explain, because of the complexity of the mechanisms underlying the mitochondrial population modulation by thyroid hormone. However, available data suggest that such a modulation occurs through changes in the turnover of the mitochondrial fractions to which an induction of mitochondrial protein synthesis and accelerated antioxidant-sensitive degradation contribute in different measure.

show abstract

“…The decrease of the heavy fraction mitochondrial characterized by high rate of oxygen consumption and the increase of the light fraction with low respiratory capacity should lead to a reduced ROS production. It is, however, likely that this change does not last long because of high synthetic ability of light mitochondrial fraction and then of their quick development into the heavy fractions [29].…”

Section: Discussionmentioning

confidence: 99%

Effect of Phenobarbital Treatment on Characteristics Determining Susceptibility to Oxidants of Homogenates, Mitochondria and Microsomes from Rat Liver

Venditti¹,

Daniele²,

Leo³

et al. 1998

Cell Physiol Biochem

View full text Add to dashboard Cite

This study was designed to investigate the possible oxidative changes associated with alterations in cytochrome P₄₅₀ levels in rat liver. Accordingly, extent of peroxidative processes, cytochrome and antioxidant content, capacity to face an oxidative stress were determined in liver microsomes, mitochondria, and homogenates from normal and phenobarbital (PB)-treated rats. Liver content of microsomal and mitochondrial proteins was also determined by the values of the activities of marker enzymes (glucose-6-phosphatase and cytochrome oxidase, respectively) in liver homogenate and in two cellular fractions. The increase in the liver content of microsomal and mitochondrial proteins indicated that PB caused proliferation of both smooth endoplasmic reticulum and mitochondrial population. Treatment with PB also gave rise to a general increase in peroxidative reactions (evaluated measuring malondialdehyde and hydroperoxides (HPs)), in the different cell compartments, even though HPs were not found significantly increased in mitochondrial fraction. The increase in peroxidative processes was associated with significant decreases in antioxidant concentration (expressed in terms of equivalent concentration of an antioxidant, such as the desferrioxamine), in all preparations from PB-treated rats. The response to oxidative stress in vitro (evaluated determining the parameters characterizing light emission from preparations stressed with sodium perborate) showed a substantial PB-induced increase in the susceptibility to oxidative challenge only in liver homogenate. The lack of changes in the mitochondrial preparations is likely due to decrease in concentration of both free radical producing species and antioxidants. The lack of changes in microsomal fraction is apparently in contrast with its lower oxidant capacity and higher content of cytochromes which are able to determine sensitivity to pro-oxidants. However, it could be due to the ability of cytochrome P₄₅₀ to interact with the active oxygen species formed at its active center.

show abstract

Heterogeneity of rat liver mitochondrial fractions and the effect of tri-iodothyronine on their protein turnover

Cited by 56 publications

References 40 publications

Impaired mitochondrial oxidative energy metabolism following paracetamol‐induced hepatotoxicity in the rat

Impaired mitochondrial oxidative energy metabolism following paracetamol‐induced hepatotoxicity in the rat

Antioxidant-Sensitive Triiodothyronine Effects on Characteristics of Rat Liver Mitochondrial Population

Effect of Phenobarbital Treatment on Characteristics Determining Susceptibility to Oxidants of Homogenates, Mitochondria and Microsomes from Rat Liver

Contact Info

Product

Resources

About