Cited by 26Aluminum toxicity and tolerance in plants and animalsHeavy Metal Exposure and ToxicityCardiac electrophysiology and arrhythmias

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Effects of diabetes mellitus and aluminum toxicity on myocardial calcium transport

Abstract

Diabetics have an increased risk of developing renal insufficiency, as well as congestive heart failure independent of coronary atherosclerotic or hypertensive heart disease. Aluminum toxicity is being recognized with increased frequency in patients with reduced renal function and aluminum accumulates to a greater degree in tissues of patients with diabetes. Studies in patients with end stage renal disease have implicated aluminum overload as a potential cause of reduced cardiac function. Since both diabetes and aluminum decrease the activity of (Ca + Mg)-ATPase, a key enzyme involved in myocardial calcium transport, the interaction of experimental diabetes mellitus and aluminum toxicity on myocardial sarcoplasmic reticulum calcium transport was investigated in rats. Aluminum alone had no effect on (Ca + Mg)-ATPase activity, while activities in both the diabetic ([DM]) and diabetic plus aluminum loaded ([DM + Al]) groups were significantly lower than controls ([C]). Oxalate-dependent calcium uptake in the [DM] rats was slightly, but not significantly lower than controls, however, uptake was markedly reduced in rats which were both diabetic and aluminum loaded. The calcium regulatory protein calmodulin was measured by a functional assay in the soluble fraction of myocardial tissue prepared from each of the four groups. Compared to [C], calmodulin activity was significantly reduced in both the [DM] and [DM + Al] groups but not affected by aluminum alone. These data indicate that diabetes mellitus is associated with decreased myocardial calmodulin activity that may contribute to reduced sarcoplasmic reticulum (Ca + Mg)-ATPase and calcium transport activities and that aluminium toxicity potentiates the adverse effects of diabetes on decreasing sarcoplasmic reticulum calcium uptake.

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  • Myocardial function may be altered in diabetic individuals by Al exposure, in as much as Al toxicity potentiates the decline in calcium uptake into the sarcoplasmic reticulum of the myocardial fibers of such individuals.

    “Myocardial function may be altered in diabetic individuals by Al exposure, in as much as Al toxicity potentiates the decline in calcium uptake into the sarcoplasmic reticulum of the myocardial fibers of such individuals (Levine et al., 1990).”

    From Aluminium toxicosis: a review of toxic actions and effects (2019) · cites this paper as Levine et al., 1990

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Research works printed but not linked: 36

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Cited by

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  • Aluminium toxicosis: a review of toxic actions and effects

    Igbokwe, I. O., Igwenagu, E., & Igbokwe, N. A. (2019) · Interdisciplinary Toxicology · doi:10.2478/intox-2019-0007 · Cited by 395

    “Myocardial function may be altered in diabetic individuals by Al exposure, in as much as Al toxicity potentiates the decline in calcium uptake into the sarcoplasmic reticulum of the myocardial fibers of such individuals (Levine et al., 1990).”
    Background

Metadata

Authors
Levine, S. N., Sonnier, G. B., & Abreo, K.
Affiliations
Louisiana State University (US)
Venue
Toxicology
Publisher
Elsevier BV
Published
1990-12
Volume
65
Issue
1-2
Pages
137-148
ISSN
0300-483X (ISSN-L)
OpenAlex
W2060804174
Cited by
26
References
0
Citations by year
2025: 1 · 2024: 2 · 2023: 3 · 2022: 2 · 2019: 1 · 2018: 1 · 2013: 1 · 2012: 1
FWCI
2.02
Type
journal article
Language
en
Open access
closed
Locations
  • Toxicology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • American Diabetes Association
  • American Heart Association
Topics
  • Life Sciences › Agricultural and Biological Sciences › Plant Science › Aluminum toxicity and tolerance in plants and animals
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Heavy Metal Exposure and Toxicity
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
Keywords
diabetes mellitus, aluminum toxicity, sarcoplasmic reticulum calcium uptake, Ca2+-Mg2+-ATPase, calmodulin, end-stage renal disease, congestive heart failure, renal failure, cardiac function
MeSH terms
Calcium-Transporting ATPases, Adenosine Triphosphate, Aluminum, Animals, Biological Transport, Blood Glucose, Body Weight, Calcium, Calmodulin, Chromatography, Affinity, Diabetes Mellitus, Experimental, Heart, Glycated Hemoglobin, Male, Microsomes, Myocardium, Organ Size, Rats, Inbred Strains, Sarcoplasmic Reticulum, Ca(2+) Mg(2+)-ATPase, Rats

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