Properties of liver mitochondria from iron-loaded rats

Hanstein, Walter G.; Sacks, Peter V.; Müller‐Eberhard, Ursula

doi:10.1016/0006-291x(75)90797-4

Cited by 37 publications

(10 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There is a small and statistically insignificant fall in the total level of malate dehydrogenase in iron overload. Similarly, the claim by Hanstein et al (1975) that mitochondria accumulate from 10-to 20-fold excess of iron in iron overloaded rats is not supported by the present studies. Inspection of the centrifugation data indicates a selective loss of the mitochondrial component which is reversed by iron depletion.…”

Section: Discussioncontrasting

confidence: 99%

“…Wattiaux de Doninck, 1970). Similarly, the claim by Hanstein et al (1975) that mitochondria accumulate from 10-to 20-fold excess of iron in iron overloaded rats is not supported by the present studies. Similar experiments to those reported by Hanstein et a/ (1975) followed by centrifugal analysis showed no increase in mitochondrial density (C. Selden & T. J. Peters, unpublished result) which would have been expected if so much iron was accumulated by this organelle.…”

Section: Discussioncontrasting

confidence: 99%

“…However, this enzyme has a dual localization to both the mitochondria and cytosol. Similar experiments to those reported by Hanstein et a/ (1975) followed by centrifugal analysis showed no increase in mitochondrial density (C. Selden & T. J. Peters, unpublished result) which would have been expected if so much iron was accumulated by this organelle. This result would suggest that slightly impaired mitochondrial function is likely in haemochromatosis.…”

Section: Discussionsupporting

confidence: 85%

See 2 more Smart Citations

Organelle Pathology in Primary and Secondary Haemochromatosis with Special Reference to Lysosomal Changes

Seymour

1978

Br J Haematol

103

View full text Add to dashboard Cite

The organelle pathology of liver biopsy specimens from patients with either primary or secondary haemochromatosis was investigated by analytical subcellular fractionation in combination with enzymic microanalysis. The most striking changes were found in the lysosomes. Increased total activities but decreased latent activities of enzymes selectively localized to the high density population of lysosomes was demonstrated in the iron overloaded biopsies. Depletion of the iron, where possible, by venesection was accompanied by a return to normal of these changes. The other subcellular organelles, plasma membrane, endoplasmic reticulum, biliary canaliculi, mitochondria, peroxisomes and the low density population of lysosomes appear to be relatively unaffected. The minor changes demonstrated are similar to those seen in other forms of chronic liver disease. It is suggested that iron mediated lysosomal disruption is implicated in the pathogenesis of the tissue damage in haemochromatosis.

show abstract

Section: Discussioncontrasting

confidence: 99%

Section: Discussioncontrasting

confidence: 99%

Section: Discussionsupporting

confidence: 85%

See 1 more Smart Citation

Organelle Pathology in Primary and Secondary Haemochromatosis with Special Reference to Lysosomal Changes

Seymour

1978

Br J Haematol

103

View full text Add to dashboard Cite

show abstract

“…(1994) thoroughly reviewed the role of iron in mitochondrial lipids, proteins and mtDNA. Several studies provide additional evidence that abnormal iron results in the significant decay of mitochondria (Hanstein et al ., 1975; Walter et al ., 2002). Similarly, excessive iron may degrade mtRNA, leading to cumulative mtRNA damage that could play a role in mitochondrial senescence.…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial iron accumulation with age and functional consequences

et al. 2008

View full text Add to dashboard Cite

Summary During the aging process, an accumulation of non-heme iron disrupts cellular homeostasis and contributes to the mitochondrial dysfunction typical of various neuromuscular degenerative diseases. Few studies have investigated the effects of iron accumulation on mitochondrial integrity and function in skeletal muscle and liver tissue. Thus, we isolated liver mitochondria (LM), as well as quadriceps-derived subsarcolemmal mitochondria (SSM) and interfibrillar mitochondria (IFM), from male Fischer 344× Brown Norway rats at 8, 18, 29 and 37 months of age. Non-heme iron content in SSM, IFM and LM was significantly higher with age, reaching a maximum at 37 months of age. The mitochondrial permeability transition pore (mPTP) was more susceptible to the opening in aged mitochondria containing high levels of iron (i.e. SSM and LM) compared to IFM. Furthermore, mitochondrial RNA oxidation increased significantly with age in SSM and LM, but not in IFM. Levels of mitochondrial RNA oxidation in SSM and LM correlated positively with levels of mitochondrial iron, whereas a significant negative correlation was observed between the maximum Ca2+ amounts needed to induce mPTP opening and iron contents in SSM, IFM and LM. Overall, our data suggest that age-dependent accumulation of mitochondrial iron may increase mitochondrial dysfunction and oxidative damage, thereby enhancing the susceptibility to apoptosis.

show abstract

“…Reissmann & Coleman (1955) presented that mitochondrial damage was associated with the development of lactic acidosis following acute intestinal iron intoxication, suggesting toxicity to Kreb's cycle enzymes. Moreover, Hanstein et al (1975) andBacon et al (1985) performed the experiments in iron loaded rats, and they suggested a cause and effect relationship between iron-induced lipid peroxidation and impaired mitochondrial function. Other morphologic alterations resulting from cell injury were liver cell ballooning with distortion and blunting of microvilli seen in some cases.…”

Section: Discussionmentioning

confidence: 99%

Liver injury due to iron overload in thalassemia: histopathologic and ultrastructural studies

Fucharoen

Boonyaphipat

et al. 1996

Biometals

View full text Add to dashboard Cite

The livers of 30 cases of thalassemia (19/beta-thal/HbE, seven thal/HbH and four beta-thal major) were studied histopathologically and electron microscopically, in an effort to define the morphologic alterations due to iron overload. The results of light and electron microscopy were similar in most cases. Iron accumulation and fibrosis were the common features found in these patients, except that thal/HbH exhibited lesser hepatic damage. The degrees of iron deposition and fibrosis were found to be higher in splenectomized and cirrhotic than non-splenectomized and non-cirrhotic patients. The subcellular changes were swollen mitochondria, with the presence of an electron dense matrix and ruptured mitochondrial membrane. Proliferation of smooth endoplasmic reticulum (ER) and dilated rough ER was observed. Increases in lysosomal hemosiderin in hepatocytes and in Kupffer cells were demonstrated. The possible ways by which the iron compounds or free radicals mediated membrane damage are mentioned. The pattern of liver cell damage is similar to that of viral hepatitis.

show abstract

Properties of liver mitochondria from iron-loaded rats

Cited by 37 publications

References 24 publications

Organelle Pathology in Primary and Secondary Haemochromatosis with Special Reference to Lysosomal Changes

Organelle Pathology in Primary and Secondary Haemochromatosis with Special Reference to Lysosomal Changes

Mitochondrial iron accumulation with age and functional consequences

Liver injury due to iron overload in thalassemia: histopathologic and ultrastructural studies

Contact Info

Product

Resources

About