Redistribution of subcellular calcium and its effect on apoptosis in primary cultures of rat proximal tubular cells exposed to lead

Wang, Hong; Wang, Zhong-Kun; Jiao, Peng; Zhou, Xiaohua; Yang, Du-Bao; Wang, Zhenyong; Wang, Lin

doi:10.1016/j.tox.2015.04.015

Cited by 45 publications

(32 citation statements)

References 31 publications

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“…The accumulation of Hg 2+ in renal tubular cells, primarily those of the proximal tubule, occurs rapidly with approximately 50% of a nontoxic dose found in the kidneys after a few hours of exposure [275,282]. Organic forms of mercury, which primarily affect the central nervous system, may also have serious toxicological effects in the kidney [283,284,285,286]. It is important to note that within biological systems, mercurous, mercuric, or methylmercuric ions do not exist as inorganic salts, or in an unbound, “free” ionic state [287].…”

Section: Environmentally Relevant Toxic Metalsmentioning

confidence: 99%

“…Exposure to all forms of mercury can have nephrotoxic effects [283,284,285,286]; however exposure to conjugates of Hg 2+ leads to the most severe nephropathy. The pars recta of the proximal tubule appears to be the most sensitive to the toxic effects of mercury and is usually the first segment of the nephron affected by exposure to mercuric compounds [275].…”

Section: Environmentally Relevant Toxic Metalsmentioning

confidence: 99%

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Chronic Kidney Disease and Exposure to Nephrotoxic Metals

Orr

Bridges

2017

IJMS

304

110

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Chronic kidney disease (CKD) is a common progressive disease that is typically characterized by the permanent loss of functional nephrons. As injured nephrons become sclerotic and die, the remaining healthy nephrons undergo numerous structural, molecular, and functional changes in an attempt to compensate for the loss of diseased nephrons. These compensatory changes enable the kidney to maintain fluid and solute homeostasis until approximately 75% of nephrons are lost. As CKD continues to progress, glomerular filtration rate decreases, and remaining nephrons are unable to effectively eliminate metabolic wastes and environmental toxicants from the body. This inability may enhance mortality and/or morbidity of an individual. Environmental toxicants of particular concern are arsenic, cadmium, lead, and mercury. Since these metals are present throughout the environment and exposure to one or more of these metals is unavoidable, it is important that the way in which these metals are handled by target organs in normal and disease states is understood completely.

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Section: Environmentally Relevant Toxic Metalsmentioning

confidence: 99%

Section: Environmentally Relevant Toxic Metalsmentioning

confidence: 99%

Chronic Kidney Disease and Exposure to Nephrotoxic Metals

Orr

Bridges

2017

IJMS

304

110

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“…27 Furthermore, previous studies have shown that the elevation of [Ca 2+ ] concentration in Pb-exposed rPT cells could evoke apoptosis induced by impaired calcium homeostasis. 35 These aforementioned studies proved that the Cd exposure caused hepatic cell death chiey through the necrotic pathway in addition to the oxidative stress impairments. 38 The typical mode of cell death is apoptosis, but necrosis has also been observed.…”

Section: Discussionmentioning

confidence: 96%

“…The density of each band was normalized to its respective loading control (b-actin). 35 The signal was detected using X-ray lms (TransGen Biotech Co., Beijing, China). The optical density (OD) of each band was determined using an Image VCD gel imaging system, and the relative abundance of PPARa, P-JNK, JNK and AMPKa1 proteins was calculated and presented as the ratios of OD of each of these proteins to that of b-actin.…”

Section: Western Blot Analysis Of Protein Levelsmentioning

confidence: 99%

Antagonistic effects of selenium against necroptosis injury via adiponectin-necrotic pathway induced by cadmium in heart of chicken

et al. 2017

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Cadmium (Cd) is one of the most toxic heavy metals having a destructive impact on various organ systems.For example, it induces oxidative stress in heart of chicken. Selenium (Se), in the form of selenoproteins, is known to protect tissues and organs against such heavy metal induced-damage. However, the precise cellular mechanism of the ameliorative role of Se in preventing Cd-induced toxicity in cardiac tissues remains unclear. The aim of this study is to investigate the role of Se in preventing Cd-induced toxicity in the chicken heart and assess the possible cytoprotective mechanism of Se. A total of 128 chickens were divided into four trial groups fed by a standard diet comprising Se, Se + , Cd + , and Se + + Cd + for 90 days.qPCR and western blotting were performed to observe the mRNA and protein expression of genes.Correlation analysis (PPI) and heat maps were used for further analysis. The results revealed that the exposure to Cd significantly increased (p < 0.05) the mRNA and protein levels of c-Jun N-terminal kinase (JNK), phosphorylated c-Jun N-terminal kinase (P-JNK), tumor necrosis factor a (TNFa), protein kinase superfamily protein 1 (RIPK1) and mixed lineage kinase domain like pseudokinase (MLKL) in the chicken. On the contrary, the mRNA and protein expression of peroxisome proliferator activated receptor alpha (PPARa), adiponectin (ADIPOQ), adiponectin receptor 1 (AdipoR1), adiponectin receptor 2 (AdipoR2), and adenosine monophosphate-activated protein kinase alpha 1 (AMPKa1) were significantly decreased in the Cd + group. Furthermore, the mRNA and protein expression levels of PPARa, adiponectin, adipoR1, adipoR2 and AMPK1 were increased (p < 0.05) significantly in the Se + group.However, the expression of JNK, TNFa and RIPK1 was significantly decreased as compared to that in the group provided with a normal standard diet. Notably, no significant increase in JNK, TNFa, RIPK1 and MLKL expression levels were observed in the chickens provided with a diet comprising Se + + Cd + , whereas the expression levels of PPARa, adiponectin, adipoR1, adipoR2 and AMPK1 were increased significantly as compared to those in the Cd + group. These results evidently indicated that Cd could induce severe myocardial damage by activating the necroptosis pathway, whereas Se could play an excellent potential role in preventing Cd-induced myocardial damage through activating adiponectin pathway.

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“…This affinity is due to an approximation of the radii of two elements and to the fact of both directions of the same electric charge. This can be attributed to one of the main types of binding in the outer layer, which favors adaptation to the same binding sites (WANG et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Effect of the use of golden mussel flour contaminated with lead as a source of calcium on the performance of broilers

Wachholz

Nunes

Gonçalves

et al. 2019

SCA

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The objective of this study was to evaluate the use of lead contaminated golden mussel flour (GMF) as a source of calcium for broiler chickens from 14 to 42 days of age and to verify the probable effects on performance, tissue contamination, blood parameters, Pb digestibility, and bone quality. The experiment was conducted in a completely randomized design (DIC), with four levels of Pb contamination (71.33, 147.55, 223.78, and 300 mg kg-1 Pb) in GMF, with five replicates and three birds per experimental unit. Sixty-four-day-old Cobb male broilers housed in metabolism cages were used. GMF was added to rations instead of calcitic limestone. The zootechnical variables were evaluated: feed intake, weight gain, and feed conversion, as well as the digestibility of nutrients. In addition, the serum biochemistry of the birds transaminases, total bilirubin, calcium, and phosphate was studied and the concentration of lead in the tissues and the bone quality of the birds was determined. The tibia was collected for evaluation of bone quality. The levels of Pb contamination in the golden mussel did not change the performance of the birds (P ? 0.05) or the Pb levels in the muscle Pectoralis major, skin, liver, feather, bones, and serum, or the serum levels of ALT, GGT, and total bilirubin, however, there was an effect of Pb levels (P < 0.01) on AST concentrations. Pb levels altered the values (P < 0.01) of the apparent digestible Pb and the coefficient of apparent digestibility of Pb, with an increasing linear effect. There was no effect (P ? 0.05) on bone stiffness, however flexibility and bone strength were altered (P < 0.05). Serum Ca and P concentrations did not show changes (P ? 0.05) due to the use of Pb levels in GMF. In this study, it can be observed that the use of GMF with Pb up to 300 mg kg-1 as a source of Ca in broiler diets does not alter performance, however the use of GMF contaminated with Pb above 73.33 mg kg-1 promotes contamination of the tissues of the animals with Pb, making it impossible to consume the birds. It was concluded that the increase in Pb concentrations in GMF increases the digestibility and metabolism of this metal and causes an increase in the production of AST by the liver. Pb levels in GMF above 214.11 mg kg-1 impair bone strength and flexibility.

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Redistribution of subcellular calcium and its effect on apoptosis in primary cultures of rat proximal tubular cells exposed to lead

Cited by 45 publications

References 31 publications

Chronic Kidney Disease and Exposure to Nephrotoxic Metals

Chronic Kidney Disease and Exposure to Nephrotoxic Metals

Antagonistic effects of selenium against necroptosis injury via adiponectin-necrotic pathway induced by cadmium in heart of chicken

Effect of the use of golden mussel flour contaminated with lead as a source of calcium on the performance of broilers

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