Functional and structural changes in liver mitochondria of rats due to CCl4 intoxication—II

Lyachovich, V.V.; Mishin, Vladimir; Dolgov, A. V.; Jakobson, G. S.; Panov, A. V.; Ib, Tsyrlov

doi:10.1016/0006-2952(71)90272-3

Cited by 4 publications

(1 citation statement)

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“…A decrease in cytochrome c has been reported in rat liver mitochondria during CC14 intoxication. 23 However, we failed to find a decrease, which coincides with the reports of Reynolds et al, 24 and Lyachovich et al 25 who found no stimulation of respiration when cytochrome c is added to mitochondria from CC14-intoxicated rats. Normal levels of cytochrome c oxidase activity have been found in CC14-damaged mitochondria.…”

Section: Figsupporting

confidence: 88%

Restoration of hepatic mitochondria during recovery from carbon tetrachloride intoxication

Brabec

Gray

Bernstein

1974

Biochemical Pharmacology

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Abstract--During CC14 intoxication in rats, a disruption of hepatic mitochondrial structure and function occurs, which is characterized by a loss of respiratory activity, loss of phosphorylation coupled to respiration, and mitochondrial swelling, attended by loss of cristae structure. Within 15-25 hr, after full development of the mitochondrial lesion, the function and structure of the mitochondria are largely restored. Studies of the turnover of mitochondrial DNA and the rates of synthesis of mitochondrial DNA and protein indicated that the CC14-insulted hepatocyte is repairing the mitochondrial damage by the insertion of specific elements into the damaged organelle, rather than by proliferation of undamaged mitochondria for replacement. The failure of ethidium bromi~e, oxytetracycline and chloramphenicol, specific inhibitors of mitochondrial protein, and/or nucleic acid synthesis, to block this restoration substantiates the postulated repair process, and also indicates the non-critical nature of the respective mitochondrial functions during the repair process. Cytochrome measurements made during the period of acute damage revealed normal levels of cytochrome c, c~ and aa a. The observed elevation of cytoehrome b is attributed to contamination of the preparation by hemoglobin.THE HEPATIC mitochondrion is one of the characteristic sites of CC14-induced cell damage. 1 Ultrastructurally, the mitochondria of an intoxicated animal appear to be swollen in situ, and the matrix is abnormally lucid. 2 The mitochondria are calcium loaded, and amorphic, dense bodies, probably aggregations of calcium phosphate, are noted in the matrix of the swollen organelles, a The altered in situ appearance is accompanied by a loss of respiratory activity, especially on NAD ÷ -linked substrates, and by an impairment of energy-coupled functions, which is detectable when isolated mitochondria are assayed. 4 This lesion is not necessarily associated with lethality, since the lesion can be developed by a dose of CC14 from which the animal recovers. Under such conditions, mitochondrial degeneration ceases and a return of normal structure and function is observed.Of interest to this laboratory is the route by which the CC14-damaged hepatocyte affects the restoration of its damaged mitochondria. In consideration of recent proposals related to mitochondrial biogenesis, it is necessary to consider a minimum of three possible routes of restoration: (1) Replacement of damaged organelles. Since it is possible that all mitochondria within a surviving hepatocyte have not suffered massive damage, a replicative burst of mitochondrial biogenesis by the slightly damaged, or undamaged mitochondria could serve to replenish the mitochondrial B,P. 23/23--A 3227

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Section: Figsupporting

confidence: 88%