Nephroprotective effect of calcium channel blockers against toxicity of lead exposure in mice

Zhang, Jianping; Cao, Hua; Zhang, Ying; Zhang, Yuanyuan; Ma, Jinlu; Wang, Jiangyan; Gao, Yanni; Zhang, Xuan; Zhang, Fenghua; Chu, Li

doi:10.1016/j.toxlet.2013.02.005

Cited by 48 publications

(25 citation statements)

References 34 publications

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“…Generally, mechanism of Pb nephrotoxicity is ascribed to the action of oxidative stress and apoptosis (Wang et al, 2009;Liu et al, 2012;Zhang et al, 2013). Our research group found that oxidative stress-mediated apoptotic death played a key role in Pb-induced nephrotoxicity in vitro.…”

Section: Introductionmentioning

confidence: 75%

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

Wang

Jiao

et al. 2015

Toxicology

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Section: Introductionmentioning

confidence: 75%

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

Wang

Jiao

et al. 2015

Toxicology

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“…3 Lead damages cellular material and produces oxidative stress by increased production of free radicals and decreased availability of antioxidant reserves. 4 It also interrupts enzyme activation and competitively inhibits trace mineral absorption. Lead poisoning may also cause reduction in renal excretion of 6-Quito-prostaglandin factor 1-alpha (a vasodilator), enhanced excretion of thromboxane (a vasoconstrictor) which make the kidney more vulnerable or prone to inflammation and favours the nephrotoxicity.…”

Section: Introductionmentioning

confidence: 99%

Nephroprotective Effect of Low Viscosity Sodium Alginate on Lead Acetate-Induced Nephrotoxicity in Rats

Kaur¹,

Sharma²

2017

IJPER

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Objective: Renal failure in majority of population is considered to be idiopathic. Heavy metals like lead in drinking water are usually the hidden cause of these renal consequences. Thus, this study has been designed to investigate the effect of low viscosity sodium alginate (LvSA) in Lead-induced nephrotoxicity. Methods: Lead (0.2% lead acetate in drinking water for 5 weeks) was administered in rats to produce nephrotoxicity assessed in terms of histopathological changes, increase in serum creatinine, blood urea nitrogen, urinary N-acetyl-β D glucosaminidase (NAG), proteinuria, Thiobarbituric acid reactive substances (TBARS) and decrease in reduced glutathione level. Results : Lead acetate (LA) intoxication shown elevations in serum creatinine, Proteinuria, glomerular filtration rate (GFR), blood urea nitrogen (BUN), Thiobarbituric acid reactive substances (TBARS), altered urinary N-acetyl-β D glucosaminidase (NAG), kidney weight/ body weight ratio (KW/BW %), and creatinine clearance that indicate renal damage. Treatment with Low viscosity sodium alginate (LvSA) show significant decrease in serum creatinine, BUN, urinary NAG, protein in urine, KW/BW %, TBARS level and increase in GSH, creatinine clearance and GFR. Conclusion: Thus, on the basis of results it may be concluded that LvSA significantly attenuated Lead-induced nephrotoxicity.

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“…It has also been proposed that agents which inhibit Ca 2+ elevations also inhibit the production of inflammatory mediators such as NO, tumor necrosis factor (TNF)-α, and interleukin-1 (IL-1) (Hattori et al 1995;Hottchkiss and Kark 1994). Diltiazem, a benzothiazepine class of CCBs, has been proposed to be effective in traumatic brain injury, short-and long-term retention c y a n i d e -i n d u c e d n e u r o t o x i c i t y, i n f l a m m a t i o n , pentylenetetrazole-provoked amnesia, and lead toxicity (Gibson et al 2010;Mathangi and Namasivayam 2003;Papazova et al 2001;Zhanga et al 2013). It blocks the entry of Ca 2+ through L-type calcium channels and thus interferes with calcium signaling which is involved in amyloid toxicity (Quartermain et al 2001;Tan et al 2012).…”

Section: Introductionmentioning

confidence: 99%

Protective effect of a calcium channel blocker “diltiazem” on aluminum chloride-induced dementia in mice

Rani

Neha

Sodhi

et al. 2015

Naunyn-Schmiedeberg's Arch Pharmacol

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Many studies report that heavy metals such as aluminum are involved in amyloid beta aggregation and neurotoxicity. Further, high concentration of aluminum in the brain deregulates calcium signaling which contributes to synaptic dysfunction and halts neuronal communication which ultimately leads to the development of Alzheimer's disease. Recently, diltiazem, a calcium channel blocker clinically used in angina, is reported to decrease amyloid beta production by inhibiting calcium influx, decreasing inflammation and oxidative stress. However, the probable role of this drug in aluminum chloride (AlCl3)-induced experimental dementia is yet to be explored. Therefore, the present study is designed to investigate the effect of AlCl3-induced dementia in mice. Morris water maze test and elevated plus maze were utilized to evaluate learning and memory. Various biochemical estimations including brain acetylcholinesterase activity (AChE), brain total protein, thiobarbituric acid-reactive species (TBARS) level, reduced glutathione (GSH) level, nitrate/nitrite, and superoxide dismutase (SOD) were measured. AlCl3 significantly impaired learning and memory and increased brain AChE, brain total protein, TBARS, and nitrate/nitrite and decreased brain GSH or SOD. On the other hand, treatment with diltiazem significantly reversed AlCl3-induced behavioral and biochemical deficits. The present study indicates the beneficial role of diltiazem in AlCl3-induced dementia.

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Nephroprotective effect of calcium channel blockers against toxicity of lead exposure in mice

Cited by 48 publications

References 34 publications

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

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

Nephroprotective Effect of Low Viscosity Sodium Alginate on Lead Acetate-Induced Nephrotoxicity in Rats

Protective effect of a calcium channel blocker “diltiazem” on aluminum chloride-induced dementia in mice

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