Nephrotoxicity of CCA-treated wood: A comparative study with As2O5 and CrO3 on mice

Matos, Rita Cerejeira; Vieira, Catarina; Morais, Simone; Pereira, Maria de Lourdes; Jesus, Júlio D. Pedrosa de

doi:10.1016/j.etap.2008.11.009

Cited by 22 publications

(19 citation statements)

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“…Heavy metals can induce renal injury (Liu et al, ). The nephrotoxicity of metals was well‐described in previous studies (Matos et al, ; Liu et al, ). Pb induces tumors in different target organs but most commonly is associated with kidney cancers in rodents.…”

Section: Introductionmentioning

confidence: 57%

“…It induces several unwanted pathological changes in tissues such as heart, brain, liver and kidney (Dewanjee et al, ). The cells of proximal tubules are the principally susceptible to toxic substances because of being the first renal epithelial cells exposed to these compounds (Matos et al, ). In this study, we determined mononuclear cell infiltration, tubular degeneration, fibrosis, dilatation of Bowmann's space, hemorrhage, glomerular lobulation, and glomerular atrophy in LN treated rat kidneys.…”

Section: Discussionmentioning

confidence: 99%

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Nephrotoxic effects of lead nitrate exposure in diabetic and nondiabetic rats: Involvement of oxidative stress and the protective role of sodium selenite

Baş

Kalender

2015

Environ. Toxicol.

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Heavy metals are known to be toxic to organisms. The present study was undertaken to evaluate the protective effect of sodium selenite against lead nitrate (LN)-induced nephrotoxicity in diabetic and nondiabetic rats. Animals were divided into eight groups where the first was served as a control, whereas the remaining groups were treated with sodium selenite (1 mg/kg b.w.), LN (22.5 mg/kg b.w.) and a combination of LN and sodium selenite and diabetic forms of these groups. Changes in antioxidant enzyme activities, malondialdehide levels, serum urea, uric acid, creatinine levels, body, and kidney weights and histopathological changes were determined after 28 days. LN caused severe histopathological changes, increment in urea, uric acid, creatinine, and MDA levels, also decreasing in antioxidant enzyme activities, body, and kidney weights. In sodium selenite + LN group, we observed the protective effect of sodium selenite on examining parameters. Also diabetes caused alterations on these parameters compared with nondiabetic animals. We found that sodium selenite did not show protective effect on diabetes caused damages. As a result, LN caused nephrotoxicity and sodium selenite alleviated this toxicity but sodium selenite did not protect kidneys against diabetes mediated toxicity. Also, LN caused more harmfull effects in diabetic groups compared with nondiabetic groups. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1229-1240, 2016.

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Section: Introductionmentioning

confidence: 57%

Section: Discussionmentioning

confidence: 99%

Nephrotoxic effects of lead nitrate exposure in diabetic and nondiabetic rats: Involvement of oxidative stress and the protective role of sodium selenite

Baş

Kalender

2015

Environ. Toxicol.

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“…In this study, PbActreated mice showed increase in plasma creatinine and urea levels, which may reflect the renal failure onset [30] . Kidney plays a major role in the clearance and biotransformation of metals [31] , and therefore is considered as a primary target organ for metals induced toxicity [32] . PbAC could increase blood urea by more than one mechanism, including enhancement of proteins catabolism, conversion of ammonia to urea by induction of arginase-enzyme synthesis [33] , and inhibition of amino acids incorporation in proteins [34] .…”

Section: Resultsmentioning

confidence: 99%

Nephroprotective Effects of Berberis Vulgaris L. Total Extract on Lead Acetate-induced Toxicity in Mice

Laamech¹,

El-Hilaly²,

Fetoui³

et al. 2016

pharmaceutical-sciences

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Laamech, et al.: Berberis vulgaris Effect on Lead Nephrotoxicity in MiceThis study aimed to investigate the potential effects of Berberis vulgaris L. against lead acetate-induced nephrotoxicity in Swiss albino mice. Mice were exposed chronically to lead acetate, at a dose of 5 mg/kg, alone or in conjunction with B. vulgaris extract (25, 50, 100 and 150 mg/kg). Lead acetate administration increased lead burden in blood and kidneys, altered renal biomarkers (serum creatinine, urea and uric acid), increased malondialdehyde and protein carbonyls levels, and decreased reduced glutathione, glutathione peroxidase, catalase, and superoxide dismutase. Histological studies showed glomerular degeneration and hypercellularity. However, B. vulgaris extract co-treatment significantly and dose-dependently restored the renal parameters, antioxidant enzymes, and histopathological changes near to the normal status, mainly via its antioxidant properties and/or by preventing lead bioaccumulation. Therefore, B. vulgaris extract showed nephroprotective effects against lead-induced nephrotoxicity mainly through its antioxidant and metal chelating properties.

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“…In addition, chromium and arsenic analyses (ICP-MS and GFAAS) were used for evaluation. Acute tubular necrosis and the individual effects of those compounds were reported after administration of CCA solution (Matos et al, 2009a(Matos et al, , 2009b(Matos et al, , 2010.…”

Section: Inherent Toxicity Associated To Chemical Components In Ccamentioning

confidence: 99%

Heavy Metals and Human Health

Morais¹,

Costa²,

Pereira³

2012

Environmental Health - Emerging Issues and Practice

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Nephrotoxicity of CCA-treated wood: A comparative study with As2O5 and CrO3 on mice

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Cited by 22 publications

References 17 publications

Nephrotoxic effects of lead nitrate exposure in diabetic and nondiabetic rats: Involvement of oxidative stress and the protective role of sodium selenite

Nephrotoxic effects of lead nitrate exposure in diabetic and nondiabetic rats: Involvement of oxidative stress and the protective role of sodium selenite

Nephroprotective Effects of Berberis Vulgaris L. Total Extract on Lead Acetate-induced Toxicity in Mice

Heavy Metals and Human Health

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