The DOI matches its Crossref record.
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.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
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
Citations
Cites
No references could be resolved yet.
Research works printed but not linked: 36
- Fein, 1985, Diabetic cardiomyopathy, Prog. Cardiovasc. Dis., 27, 255, 10.1016/0033-0620(85)90009-X · DOI
- Tahiliani, 1986, Diabetes-induced abnormalities in the myocardium, Life Sci., 38, 959, 10.1016/0024-3205(86)90229-8 · DOI
- Vered, 1984, Exercise-induced left ventricular dysfunction in young men with asymptomatic diabetes mellitus (diabetic cardiomyopathy), Am. J. Cardiol., 54, 633, 10.1016/0002-9149(84)90263-7 · DOI
- McNeill, 1985, Endocrine dysfunction and cardiac performance, Can. J. Physiol. Pharmacol., 63, 1, 10.1139/y85-001 · DOI
- Macdonald, 1985, Aluminum ion in biological systems, Trends Biochem. Sci., 13, 15, 10.1016/0968-0004(88)90012-6 · DOI
- Andress, 1987, Early Deposition of aluminum in bone in diabetic patients on hemodialysis, N. Engl. J. Med., 316, 292, 10.1056/NEJM198702053160602 · DOI
- London, 1989, Association between aluminum accumulation and cardiac hypertrophy in hemodialyzed patients, Am. J. Kidney Dis., 13, 75, 10.1016/S0272-6386(89)80120-9 · DOI
- Lopaschuk, 1983, The effect of alloxan- and streptozotocin-induced diabetes on calcium transport in rat cardiac sarcoplasmic reticulum. The possible involvement of long chain acylcarnitines, Can. J. Physiol. Pharmacol., 61, 439, 10.1139/y83-068 · DOI
- Ganguly, 1983, Defective sarcoplasmic reticular calcium transport in diabetic cardiomyopathy, Am. J. Physiol. (Endocrinol. Metab. 7), 244, E528, 10.1152/ajpendo.1983.244.6.E528 · DOI
- Siegel, 1985, Aluminum interaction with biomolecules: the molecular basis for aluminum toxicity, Am. J. Kidney Dis., 5, 353, 10.1016/S0272-6386(85)80093-7 · DOI
- Lopaschuk, 1983, Characterization of cardiac microsomal sarcoplasmic reticulum prepared from control and diabetic rats, J. Pharmacol. Methods, 10, 199, 10.1016/0160-5402(83)90031-1 · DOI
- Levine, 1986, Exercise conditioning increases rat myocardial calcium uptake, J. Appl. Physiol., 60, 1673, 10.1152/jappl.1986.60.5.1673 · DOI
- Levine, 1983, Aprindine inhibits calmodulin-stimulated phosphodiesterase and Ca-ATPase activities, J. Cardiovasc. Pharmacol., 5, 151, 10.1097/00005344-198301000-00023 · DOI
- Thompson, 1974, Assay of cyclic nucleotide phosphodiesterase with radioactive substances, Methods Enzymol., 38, 205, 10.1016/0076-6879(74)38033-0 · DOI
- Abreo, 1988, Effect of 1,25-vitamin D and parathyroidectomy on the uptake of aluminum in bone of rats with renal insufficiency, Am. J. Nephrol., 8, 426, 10.1159/000167631 · DOI
- Lowry, 1951, Protein measurement with the Folin phenol reagent, J. Biol. Chem., 193, 265, 10.1016/S0021-9258(19)52451-6 · DOI
- Stocler, 1987, Calmodulin and its role in intracellular calcium regulation, Prog. Neurobiol., 29, 321, 10.1016/0301-0082(87)90018-9 · DOI
- Tahiliani, 1985, Prevention of diabetes-induced myocardial dysfunction in rats by methyl palmoxirate and triiodothyronine treatment, Can. J. Physiol. Pharmacol., 63, 925, 10.1139/y85-153 · DOI
- Lopaschuk, 1984, Depression of calcium transport in sarcoplasmic reticulum from diabetic rats: lack of involvement by specific regulatory mediators, Gen. Pharmacol., 15, 1, 10.1016/0306-3623(84)90071-5 · DOI
- Recker, 1977, Evidence for aluminum absorption from the gastrointestinal tract and bone deposition by aluminum carbonate ingestion with normal renal function, J. Lab. Clin. Med., 5, 810
- Krishnan, 1988, Aluminum toxicity in humans, Vol. 18, 645
- Kaiser, 1985, Aluminum-induced anemia, Am. J. Kidney Dis., 5, 348, 10.1016/S0272-6386(85)80092-5 · DOI
- Smith, 1986, Aluminum-related bone disease in mild and advanced renal failure: evidence for high prevalence and morbidity and studies on etiology and diagnoses, Am. J. Nephrol., 6, 275, 10.1159/000167175 · DOI
- Roth, 1984, Multiorgan aluminum deposits in a chronic haemodialysis patient. Electron microscope and microprobe studies, Virchows Arch. (Pathol. Anat.), 405, 131, 10.1007/BF00694931 · DOI
- Timsit, 1985, Cardiomyopathie aluminique chez un hémodialysé chronique, Néphrologie, 6, 263
- Martonosi, 1982, Transport of calcium by sarcoplasmic reticulum, Vol. 3, 38
- Kirchberger, 1982, Calmodulin-mediated regulation of calcium transport and (Ca2+ + Mg2+)-activated ATPase activity in isolated cardiac sarcoplasmic reticulum, J. Biol. Chem., 257, 5685, 10.1016/S0021-9258(19)83832-2 · DOI
- Davis, 1983, Regulation of cardiac sarcoplasmic reticulum calcium transport by calcium-calmodulin-dependent phosphorylation, J. Biol. Chem., 258, 13587, 10.1016/S0021-9258(17)43955-X · DOI
- Lindemann, 1985, Phosphorylation of phospholamban in intact myocardium: role of Ca2+-calmodulin-dependent mechanisms, J. Biol. Chem., 260, 4516, 10.1016/S0021-9258(18)89294-8 · DOI
- Gasser, 1988, Heterogeneous distribution of calmodulin and cAMP-dependent regulation of Ca2+ uptake in cardiac sarcoplasmic reticulum subfractions, Eur. J. Biochem., 176, 535, 10.1111/j.1432-1033.1988.tb14311.x · DOI
- Meissner, 1988, Biochemical characterization of the Ca2+ release channel of skeletal and cardiac sarcoplasmic reticulum, Mol. Cell. Biochem., 82, 59, 10.1007/BF00242517 · DOI
- Bkaily, 1986, Calmodulin is required for a full activation of the calcium slow channels in heart cells, J. Cyclic Nucleotide Protein Phosphor. Res., 11, 25
- Siegel, 1983, Aluminum interaction with calmodulin: evidence for altered structure and function from optical and enzymatic studies, Biochim. Biophys. Acta, 744, 36, 10.1016/0167-4838(83)90337-0 · DOI
- Richardt, 1985, The interaction of aluminum and other metal ions with calcium-calmodulin- dependent phosphodiesterase, Arch. Toxicol., 57, 257, 10.1007/BF00324788 · DOI
- Solomon, 1986, Spontaneous diabetic BB rat: studies of cyclic adenosine 3′,5′-monophosphate phosphodiesterase and calmodulin, Endocrinology, 119, 1839, 10.1210/endo-119-4-1839 · DOI
- Solomon, 1987, Inhibitor of calmodulin and cAMP phosphodiesterase activity in BB rats, Diabetes, 36, 210, 10.2337/diab.36.2.210 · DOI
Cited by
Sorted by citations
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review