Effect of ferric iron and desferrioxamine on lipofuscin accumulation in cultured rat heart myocytes

Marzabadi, Massoud R.; Sohal, Rajindar S.; Brunk, Ulf T.

doi:10.1016/0047-6374(88)90122-4

Cited by 49 publications

(22 citation statements)

References 14 publications

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“…Training or a combination of training and vitamin E proved less beneficial in the old in terms of reducing LP. These findings may relate to the concept that vitamin E can inhibit LP and reduce the accumulation of LF, which is one of the products of LP (Marzabadi et al, 1991). These results are in accordance with our earlier in vitro studies on the primary cultures of myocytes as well as neurons, wherein it was demonstrated that the AO could substantially reduce the autofluorescent substances (Asha Devi et al, 1990;Kan et al, 1991).…”

Section: Discussionsupporting

confidence: 81%

Dietary vitamin E and physical exercise: II. Antioxidant status and lipofuscin-like substances in aging rat heart

Devi

Shetty

Subramanyam

2003

Experimental Gerontology

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The heart faces a high risk of free radical injury owing to a slow generation of antioxidant (AO) enzymes by its cells. A general decline in this system may be another reason for the development of age-related diseases. Although the correlation between aging and exercise has been studied extensively, these studies have produced conflicting data on the effects of vitamin E on the aging heart, when it is introduced as an intervening factor. To investigate these effects, we determined the activities of antioxidant enzymes (AOEs) such as superoxide dismutase (SOD) and catalase (CAT), lipid peroxidation (LP), lipofuscin (LF)-like autofluorescent substances and vitamin E content in the left and right ventricles (LV and RV) of the heart in male Wistar albino rats of 4-(young adults), 8-(old adults), 12-(middle-age) and 22-mos(old) of age. Animals were orally supplemented with vitamin E and allowed to swim for 30 min/day, 5 days/week and for a total period of 60 days. Exercise training in all the age groups except the old was effective in upregulating the SOD activity. Old trainees showed an increase in SOD activity when supplemented with vitamin E. In the 22-mo-olds, a remarkable decrease in CAT activity was seen. Exercise by itself upregulated the CAT as well as SOD activity in all age groups except the old wherein vitamin E was effective in increasing the activities of AOEs. Supplementation significantly reduced LP as evidenced by lowered malondialdehyde (MDA) and LF-like autofluorescent substances in the trained as well as sedentary rats. Tissue vitamin E content was low in the swim trainees that were not supplemented. This change, well emphasized in the trainee groups of 22-mo-old suggests the probable utilization of vitamin E in keeping free radicals at bay. Our results suggest that vitamin E can stand out as a significant tool in ameliorating the declining AO defense in the old rats. q

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Section: Discussionsupporting

confidence: 81%

Dietary vitamin E and physical exercise: II. Antioxidant status and lipofuscin-like substances in aging rat heart

Devi

Shetty

Subramanyam

2003

Experimental Gerontology

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“…The two MRL strains, which exhibited no lipofuscin, were relatively resistant to lesion formation. Based on these observations, as well as data reported by others suggesting that both lipofuscin (1)(2)(3)(4)(5)(6)(7)(8)(9) and fatty streak (26) formation involve lipid oxidation, we hypothesized that these processes may exhibit coordinate control. To investigate this hypothesis, we examined the concordance of lipofuscin and fatty streak formation in ATH-fed BALB/cJ mice, which exhibit incomplete penetrance of both traits.…”

Section: Methodsmentioning

confidence: 99%

“…Oxidative stress appears to play a key role in lipofuscin formation. For example, increases in oxygen and iron concentrations act synergistically to induce lipofuscin deposition in cultured rat myocytes (4,5). Similarly, high intake ofpolyunsaturated fatty acids (6) or deficiency ofantioxidants, such as vitamin E (7,8 ), increases the rate of lipofuscin formation in tissues of experimental animals.…”

Section: Introductionmentioning

confidence: 99%

Involvement of the tyrosinase gene in the deposition of cardiac lipofuscin in mice. Association with aortic fatty streak development.

Qiao

Welch²,

Xie³

et al. 1993

J. Clin. Invest.

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Lipofuscin pigment, a terminal oxidation product, accumulates within cells during the normal aging process and under certain pathological conditions. We have analyzed a genetic cross between two inbred mouse strains, BALB/cJ and a subline of C57BL/6J, which differ in lipofuscin deposition. A comparison of the segregation pattern of cardiac lipofuscin with the albino locus (c) on mouse chromosome 7 revealed complete concordance. Analysis of spontaneous mutants of the tyrosinase gene, encoded by the albino locus, confirmed that the tyrosinase gene itself controls lipofuscin formation. Genetic analysis of other strains indicated that one or more additional genes can contribute to the inheritance of lipofuscin. We also present evidence for an association between cardiac lipofuscin deposition and aortic fatty streak development in the mouse. (J. Clin. Invest. 1993. 92:2386-2393

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“…This study, and several others, have lately shown that increase of cellular iron content obtained by exposing cell cultures to Fe 3ϩ will lead to a higher probability for hydroxyl radical formation and, thus, increased oxidative damage (12,37). Conversion of intracellular iron to a more redox active form would result in increased risk of oxidative damage (8,26,38). Since the turnover of ferritin is very rapid in the liver, it is reasonable to assume that most of the increased amounts of DFX-available iron detected was derived from ferritin.…”

Section: Discussionmentioning

confidence: 99%

Nutrient Deprivation of Cultured Rat Hepatocytes Increases the Desferrioxamine-available Iron Pool and Augments the Sensitivity to Hydrogen Peroxide

Öllinger

Roberg

1997

Journal of Biological Chemistry

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Primary cultures of rat hepatocytes were subjected to amino acid and serum deprivation for 4 h. This treatment augmented the sensitivity to ensuing hydrogen peroxide exposure for 30 min. The by nutrient deprivation-increased autophagocytosis was confirmed by transmission electron microscopy and uptake of the lysosomotropic weak base acridine orange within the intracellular acidic vacuolar apparatus. The desferrioxamine-available pool of iron increased 2.5-fold during deprivation, compared with control cells. Furthermore, amino acid deprivation increased the cellular protein turnover, measured by radioactive labeling with [ 3 H]Leu. Exposure to 40 M ascorbic acid specifically decreased the turnover of ferritin, as estimated by enzyme-linked immunosorbent assay, and prevented an increase of the desferrioxamine-available iron pool, resulting in protection against hydrogen peroxide-induced cell killing.Thus, hepatocytes with nutrient deprivation-enhanced autophagocytosis contain a larger pool of catalytically active iron than control cells. This iron pool is mainly derived from the turnover (autophagocytosis) of cytosolic ferritin and is probably situated in the lysosomes. Furthermore, nutrient-deprived cells show augmented sensitivity to hydrogen peroxide-induced oxidative stress, since the enhanced availability of iron in low molecular weight form results in an increased potential of intralysosomal Fenton chemistry, that may cause lysosomal rupture with release of potent hydrolytic enzymes.

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Effect of ferric iron and desferrioxamine on lipofuscin accumulation in cultured rat heart myocytes

Cited by 49 publications

References 14 publications

Dietary vitamin E and physical exercise: II. Antioxidant status and lipofuscin-like substances in aging rat heart

Dietary vitamin E and physical exercise: II. Antioxidant status and lipofuscin-like substances in aging rat heart

Involvement of the tyrosinase gene in the deposition of cardiac lipofuscin in mice. Association with aortic fatty streak development.

Nutrient Deprivation of Cultured Rat Hepatocytes Increases the Desferrioxamine-available Iron Pool and Augments the Sensitivity to Hydrogen Peroxide

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