Activation of troponin C by Cd2+ and Pb2+

Chao, Sheng-Hao; Bu, Chun Hui; Cheung, Wai Yiu

doi:10.1007/bf01977632

Cited by 36 publications

(29 citation statements)

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“…Radical scavenging has been related with reduction of in vitro DNA damage and lipid peroxidation and, thus, in an overall decrement in the toxic potential of the fibers. [2,16,17,36,37] Biochemical response of fungi to asbestos fibers: Modification in protein expression: The modification in protein expression following interaction with asbestos may be a fungal response either to physical contact with the fibers or to a possible oxidative stress caused by the fiber or by mobilized iron. The SEM analysis of mycelia grown in direct contact with the fibers showed the physical integrity of hyphae; [25] thus, the extracellular protein pool changes in the presence of fibers are likely to be due to active synthesis.…”

Section: Discussionmentioning

confidence: 99%

“…[13,14] Incubation of the fibers with an aqueous solution of some chelators was reported to inhibit surface reactivity [15] and to decrease DNA damage and lipid peroxidation in vitro. [16][17][18] Synthetic chrysotile with no iron in the structure was recently reported not to be cytotoxic toward human epithelial cells in a culture. [19] Iron extraction from asbestos fibers may also destabilize the lattice if the extraction proceeds for several layers below the fiber surface.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Inorganic Materials and Living Organisms: Surface Modifications and Fungal Responses to Various Asbestos Forms

Daghino

Martino

Fenoglio

et al. 2005

Chemistry A European J

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In a previous study several strains of soil fungi were reported to remove iron in vitro from crocidolite asbestos, a process that was envisaged as a possible bioremediation route for asbestos-polluted soils. Here, we get some new insight into the chemical basis of the fiber/fungi interaction by comparing the action of the most active fungal strain Fusarium oxysporum on three kind of asbestos fibers--chrysotile, amosite, and crocidolite--and on a surface-modified crocidolite. None of the fibers examined significantly inhibited biomass production. Even the smallest fibrils were visibly removed from the supernatant following adhesion to fungal hyphae. F. oxysporum, through release of chelators, extracted iron from all fibers; the higher the amount of iron at the exposed surface, the larger the amount removed, that is, crocidolite > amosite >> chrysotile. When considering the fraction of total iron extracted, however, the ranking was chrysotile > crocidolite > amosite > heated crocidolite, because of the different accessibility of the chelators to the metal ions in the crystal structure. Chrysotile was the easiest to deplete of its metal content. Iron removal fully blunted HO* radical release from crocidolite and chrysotile but only partially from amosite. The removal, in a long-term experiment, of more iron than is expected to be at the surface suggests a diffusion of ions from the bulk solid towards the surface depleted of iron by fungal activity. Thus, if the fibers could be treated with a continuous source of chelators, iron extraction would proceed up to a full inactivation of free radical release. The fungal metabolic response of F. oxysporum grown in the presence of chrysotile, amosite and crocidolite revealed that new extracellular proteins are induced--including manganese-superoxide dismutase, the typical antioxidant defense--and others are repressed, upon direct contact with the fibers. The protein profile induced by heated crocidolite was different, a result suggesting a key role for the state of the fiber/hyphae interface in protein induction.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Inorganic Materials and Living Organisms: Surface Modifications and Fungal Responses to Various Asbestos Forms

Daghino

Martino

Fenoglio

et al. 2005

Chemistry A European J

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“…Pb is an effective competitor with Ca for protein binding when equimolar concentrations are used in the test tube. 49,50 If there had been a 1000-fold difference in the molar concentrations of these metals presented to the gut, then additional Ca would not be expected to have a demonstrable additional effect on reducing absorption. This leaves open the possibility that Ca supplementation may still play a role in the treatment of Pb-poisoned children who are dietarily Ca deficient.…”

Section: Discussionmentioning

confidence: 99%

A Randomized Trial of Calcium Supplementation for Childhood Lead Poisoning

2004

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ABSTRACT. Objective. Lead (Pb) poisoning remains a common disease among children despite successful public health efforts that have reduced its prevalence. Treatment options for children with blood Pb levels (BPbs) <45 g/dL are limited because chelation therapy is generally not indicated. Calcium (Ca) and Pb interactions are well documented. Competition for binding to Ca-binding proteins may underlie a mechanism for Pb absorption. The purpose of this study was to determine the role, if any, of supplemental Ca at reducing BPbs in moderately poisoned children.Methods. Children aged 1 to 6 years with BPbs 10 to 45 g/dL were enrolled in a double-blinded, placebocontrolled trial of the effects of Ca supplementation on BPbs. Children received either a Ca-containing liquid or an indistinguishable placebo. Dosage was adjusted biweekly on the basis of responses to a dietary Ca intake questionnaire to reach 1800 mg in the Ca-supplemented group. Samples for BPbs and measures to assess safety were collected before and after 3 months of supplementation and after an additional 3 months of follow-up. Bivariate and multiple regression analyses were performed.Results. A total of 67 of 88 enrolled children with a mean age of 3.6 years completed 3 months of supplementation. There were no statistically significant differences between groups on hematologic and biochemical measures, including serum and urinary Ca, at any time points. The average compliance rate was estimated to be 80% for each group during the 3-month supplementation period.Conclusions. At enrollment, the average daily Ca intake in this group of inner-city children was greater than the recommended daily intake for age. Although BPbs declined during a 3-month period in both groups, Ca supplementation aimed at providing 1800 mg of Ca/day had no effect on the change in BPbs. Ca supplementation should not be routinely prescribed for mild to moderately Pb-poisoned children who are dietarily Ca sufficient. Pediatrics 2004;113:e34 -e39. URL: http://www. pediatrics.org/cgi/content/full/113/1/e34; lead, lead poisoning, calcium, calcium supplementation.ABBREVIATIONS. Pb, lead; BPb, blood lead level; CDC, Centers for Disease Control and Prevention; EP, erythrocyte protoporphyrin; AAS, atomic absorption spectrometry; SD, standard deviation; sCa, serum calcium; uCa, urinary calcium; uCr, urinary creatinine. C hildhood lead (Pb) poisoning is prevalent worldwide. In the United States alone, an estimated 0.5 million preschool-aged children have elevated blood Pb levels (BPbs; Ն10 g/dL). 1 The poisoning of this large number of children is, in large part, the consequence of the widespread presence of leaded paint in US residential housing. The National Academy of Sciences estimates that there are 3 million tons of leaded paint in housing built primarily before 1960. 2 Outside the US, the continued use of leaded gasoline is associated with elevated BPbs in urban populations. 3 A study completed recently in India found that average BPbs in 5 major cities were comparable to that in the U...

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“…Additionally, Chao et al reported that Pb 2+ produces a biphasic activation and inactivation of MLCK with increasing Pb 2+ concentration, but only in the presence of CaM, indicating that Pb 2+ interacts directly with CaM, not MLCK (97). Chao et al reported in a later study that Pb 2+ activated TnC, which subsequently stimulated myofibrillar ATPase (98). Therefore, the effects of Pb 2+ on different processes may occur indirectly via interactions with upstream proteins.…”

Section: Pb2+ Effects On Functional Activity Of Proteins Associated Wmentioning

confidence: 99%

“…The Pb 2+ ion can also occupy Ca 2+ -binding sites, and/or displace Ca 2+ in many proteins, including voltage-gated calcium channels (VGCCs) (140), troponin C (98), CaM (32), PKC (58), parvalbumin (64), and synaptotagmin (40). Moreover, CABPs have also been observed to bind a number of different non-essential metals in addition to Pb 2+ , including Sr 2+ , Hg 2+ , Cd 2+ and many lanthanides (141–145).…”

Section: A New Perspective For the Molecular Basis Of Pb2+ Toxicitymentioning

confidence: 99%

Defining potential roles of Pb²⁺in neurotoxicity from a calciomics approach

et al. 2016

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Metal ions play crucial roles in numerous biological processes, facilitating biochemical reactions by binding to various proteins. An increasing body of evidence suggests that neurotoxicity associated with exposure to nonessential metals (e.g., Pb2+) involves disruption of synaptic activity, and these observed effects are associated with the ability of Pb2+ to interfere with Zn2+ and Ca2+-dependent functions. However, the molecular mechanism behind Pb2+ toxicity remains a topic of debate. In this review, we first discuss potential neuronal Ca2+ binding protein (CaBP) targets for Pb2+ such as calmodulin (CaM), synaptotagmin, neuronal calcium sensor-1 (NCS-1), N-methyl-D-aspartate receptor (NMDAR) and family C of G-protein coupled receptors (cGPCRs), and their involvement in Ca2+-signalling pathways. We then compare metal binding properties between Ca2+ and Pb2+ to understand the structural implications of Pb2+ binding to CaBPs. Statistical and biophysical studies (e.g., NMR and fluorescence spectroscopy) of Pb2+ binding are discussed to investigate the molecular mechanism behind Pb2+ toxicity. These studies identify an opportunistic, allosteric binding of Pb2+ with CaM that is distinct from ionic displacement. Together, this data suggests three potential modes of Pb2+ activity related to molecular and/or neural toxicity: (i) Pb2+ can occupy Ca2+-binding sites, inhibiting the activity of the protein by structural modulation, (ii) Pb2+ can mimic Ca2+ in the binding sites, falsely activating the protein and perturbing downstream activities, or (iii) Pb2+ binds outside of the Ca2+-binding sites, resulting in allosteric modulation of the proteins activity. Moreover, the data further suggest that even low concentrations of Pb2+ can interfere at multiple points within the neuronal Ca2+ signalling pathways to cause neurotoxicity.

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Activation of troponin C by Cd2+ and Pb2+

Cited by 36 publications

References 45 publications

Inorganic Materials and Living Organisms: Surface Modifications and Fungal Responses to Various Asbestos Forms

Inorganic Materials and Living Organisms: Surface Modifications and Fungal Responses to Various Asbestos Forms

A Randomized Trial of Calcium Supplementation for Childhood Lead Poisoning

Defining potential roles of Pb²⁺in neurotoxicity from a calciomics approach

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Activation of troponin C by Cd2+ and Pb2+

Cited by 36 publications

References 45 publications

Inorganic Materials and Living Organisms: Surface Modifications and Fungal Responses to Various Asbestos Forms

Inorganic Materials and Living Organisms: Surface Modifications and Fungal Responses to Various Asbestos Forms

A Randomized Trial of Calcium Supplementation for Childhood Lead Poisoning

Defining potential roles of Pb2+in neurotoxicity from a calciomics approach

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Product

Resources

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Defining potential roles of Pb²⁺in neurotoxicity from a calciomics approach