Skip to main content
The Journal of Cell Biology logoLink to The Journal of Cell Biology
. 1969 May 1;41(2):393–400. doi: 10.1083/jcb.41.2.393

ULTRASTRUCTURAL TRANSFORMATION IN MITOCHONDRIA ISOLATED FROM KIDNEYS OF NORMAL AND LEAD-INTOXICATED RATS

R A Goyer 1, R Krall 1
PMCID: PMC2107769  PMID: 5783864

Abstract

Mitochondria isolated from kidneys of lead-intoxicated rats have been shown to have decreased oxidative and phosphorylative abilities. The purpose of this study was to determine whether these abnormal mitochondria would undergo ultrastructural transformation during controlled respiration in the absence of phosphate acceptor (State IV), as previously demonstrated for normal liver mitochondria. It was first shown that normal rat kidney mitochondria transforms from a condensed ultrastructural conformation to an orthodox conformation after 5 min of State IV respiration with pyruvate-malate substrate. Reversal to a condensed conformation follows stimulation of respiration with adenosine diphosphate (ADP). A large portion of kidney mitochondria from lead-poisoned rats do not change from condensed to orthodox conformation during State IV respiration. Other mitochondria do transform to the orthodox form but they rapidly degenerate. State IV respiration decreases as these few orthodox mitochondria disintegrate. The conclusion is that those mitochondria that do not undergo change in ultrastructure have impairment of electron transport, and that those that do become orthodox have increased membrane lability and undergo degeneration.

Full Text

The Full Text of this article is available as a PDF (893.9 KB).

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. CHANCE B., WILLIAMS G. R. Respiratory enzymes in oxidative phosphorylation. I. Kinetics of oxygen utilization. J Biol Chem. 1955 Nov;217(1):383–393. [PubMed] [Google Scholar]
  2. Goyer R. A., Krall A., Kimball J. P. The renal tubule in lead poisoning. II. In vitro studies of mitochondrial structure and function. Lab Invest. 1968 Jul;19(1):78–83. [PubMed] [Google Scholar]
  3. Goyer R. A. The renal tubule in lead poisoning. I. mMitochondrial swelling and aminoacidura. Lab Invest. 1968 Jul;19(1):71–77. [PubMed] [Google Scholar]
  4. Hackenbrock C. R. Ultrastructural bases for metabolically linked mechanical activity in mitochondria. I. Reversible ultrastructural changes with change in metabolic steady state in isolated liver mitochondria. J Cell Biol. 1966 Aug;30(2):269–297. doi: 10.1083/jcb.30.2.269. [DOI] [PMC free article] [PubMed] [Google Scholar]
  5. Hackenbrock C. R. Ultrastructural bases for metabolically linked mechanical activity in mitochondria. II. Electron transport-linked ultrastructural transformations in mitochondria. J Cell Biol. 1968 May;37(2):345–369. doi: 10.1083/jcb.37.2.345. [DOI] [PMC free article] [PubMed] [Google Scholar]
  6. Jasper D. K., Bronk J. R. Studies on the physiological and structural characteristics of rat intestinal mucosa. Mitochondrial structural changes during amino acid absorption. J Cell Biol. 1968 Aug;38(2):277–291. doi: 10.1083/jcb.38.2.277. [DOI] [PMC free article] [PubMed] [Google Scholar]
  7. Mintz H. A., Yawn D. H., Safer B., Bresnick E., Liebelt A. G., Blailock Z. R., Rabin E. R., Schwartz A. Morphological and biochemical studies of isolated mitochondria from fetal, neonatal, and adult liver and from neoplastic tissues. J Cell Biol. 1967 Aug;34(2):513–523. doi: 10.1083/jcb.34.2.513. [DOI] [PMC free article] [PubMed] [Google Scholar]

Articles from The Journal of Cell Biology are provided here courtesy of The Rockefeller University Press

RESOURCES