Uptake of inorganic lead in vitro by isolated mitochondria and tissue slices of rat renal cortex

Kapoor, Shiv; Rossum, G.D.V. Van; O’Neill, Kevin; Mercorella, Isabella

doi:10.1016/0006-2952(85)90682-3

Cited by 18 publications

(13 citation statements)

References 24 publications

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“…Lead inhibits uptake of calcium into isolated renal mitochondria and may enter mitochondria as a substrate for a calcium transporter (Kapoor et al 1985). This would be consistent with evidence that lead can interact with calcium binding proteins and thereby affect calciummediated or regulated events in a variety of tissues (Fullmer et al 1985;Goldstein 1993;Goldstein and Ar 1983;Habermann et al 1983;Platt and Busselberg 1994;Pounds 1984;Richardt et al 1986;Rosen and Pounds 1989;Simons and Pocock 1987;Sun and Suszkiw 1995;Tomsig and Suszkiw 1995;Watts et al 1995).…”

Section: Renal Effects Lead In Cells Binds To a Variety Of Proteinssupporting

confidence: 74%

Characterizing Golden Eagle Risk to Lead and Anticoagulant Rodenticide Exposure: A Review

Herring

Eagles‐Smith

Buck

2017

Journal of Raptor Research

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Section: Renal Effects Lead In Cells Binds To a Variety Of Proteinssupporting

confidence: 74%

Characterizing Golden Eagle Risk to Lead and Anticoagulant Rodenticide Exposure: A Review

Herring

Eagles‐Smith

Buck

2017

Journal of Raptor Research

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“…Lead exposure alters the mitochondrial structure in tissues taken from lead-intoxicated animals and in human biopsy specimens (Goyer 1968; Goyer et al 1968). Competing with calcium, lead is taken up into mitochondria in an energy dependent manner (Walton 1973; Walton and Buckley 1977; Kapoor et al 1985). Future studies are needed to determine if the differences in expression of the mitochondrial genes that correlate with lead in AU compared to control children translate into dys-regulated mitochondrial function in AU.…”

Section: Discussionmentioning

confidence: 99%

Correlations of Gene Expression with Blood Lead Levels in Children with Autism Compared to Typically Developing Controls

et al. 2009

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The objective of this study was to examine the correlation between gene expression and lead (Pb) levels in blood in children with autism (AU, n = 37) compared to typically developing controls (TD, n = 15). We postulated that, though lead levels did not differ between the groups, AU children might metabolize lead differently compared to TD children. RNA was isolated from blood and processed on Affymetrix microarrays. Separate analyses of covariance (ANCOVA) corrected for age and gender were performed for TD, AU, and all subjects (AU + TD). To reduce false positives, only genes that overlapped these three ANCOVAs were considered. Thus, 48 probe sets correlated with lead levels in both AU and TD subjects and were significantly different between the groups (p(Diagnosis × log2 Pb) < 0.05). These genes were related mainly to immune and inflammatory processes, including MHC Class II family members and CD74. A large number (n = 791) of probe sets correlated (P ≤ 0.05) with lead levels in TD but not in AU subjects; and many probe sets (n = 162) correlated (P ≤ 0.05) with lead levels in AU but not in TD subjects. Only 30 probe sets correlated (P ≤ 0.05) with lead levels in a similar manner in the AU and TD groups. These data show that AU and TD children display different associations between transcript levels and low levels of lead. We postulate that this may relate to the underlying genetic differences between the two groups, though other explanations cannot be excluded.Electronic supplementary materialThe online version of this article (doi:10.1007/s12640-009-9126-x) contains supplementary material, which is available to authorized users.

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“…Researchers who carried out studies on the mitochondria from the retinal rod cells, however, came to an opposite conclusion [36]. Kapoor et al [37], in turn, found that lead-induced swelling of the mitochondria from the rat renal cortex is realized only in 30-50% of the cases. Considering other published data, we can conclude that there is indirect evidence in favor of just our own findings.…”

Section: Resultsmentioning

confidence: 96%

Mechanisms underlying interaction of zinc, lead, and cobalt with nonspecific permeability pores in the mitochondrial membranes

Kravenskaya

Fedirko

2011

Neurophysiology

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It was demonstrated that Zn 2+ , in contrast to Pb 2+ and Со 2+ , initiates the development of the nonspecific mitochondrial permeability (NMP) in hepatocytes. Kinetic analysis of this process was performed. It was proved that Zn-induced NMP is mediated by activation of megachannels (mitochondrial permeability transition pores). Sulfo groups of the ADP/ATP antiporter and carboxylic groups of voltage-dependent anionic channels are also involved in the development of Zn 2+ -stimulated NMP. Interaction between Zn 2+ and cyclophilin D is the key event in the process of activation of NMP. We found that the Na/Ca exchanger exerts an activating effect on the Zn-induced NMP. In general, swelling of the mitochondria and Ca 2+ release from these organelles under the action of Zn 2+ are based on noticeably dissimilar mechanisms. The observed distinctions depend on the functional state of the mitochondrial transport systems.

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Uptake of inorganic lead in vitro by isolated mitochondria and tissue slices of rat renal cortex

Cited by 18 publications

References 24 publications

Characterizing Golden Eagle Risk to Lead and Anticoagulant Rodenticide Exposure: A Review

Characterizing Golden Eagle Risk to Lead and Anticoagulant Rodenticide Exposure: A Review

Correlations of Gene Expression with Blood Lead Levels in Children with Autism Compared to Typically Developing Controls

Mechanisms underlying interaction of zinc, lead, and cobalt with nonspecific permeability pores in the mitochondrial membranes

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