Exposure to arsenite and cadmium induces organotoxicity and miRNAs deregulation in male rats

Mumtaz, Farah; Albeltagy, Rasha S; Diab, Marwa S.M.; Moneim, Ahmed E. Abdel; El-Habit, Ola H.

doi:10.1007/s11356-020-08306-1

Cited by 19 publications

(11 citation statements)

References 60 publications

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“…It is used in the manufacturing of semiconductors, dyes, wood preservatives, glass, and agricultural pesticides. 1 This hazardous metal is considered as a potent environmental toxic agent, and chronic small-dose arsenic exposure represents a major concern owing to its carcinogenic effects on human populations. Workers in the industries mentioned above face potential exposure to the poisonous effects of As.…”

Section: Introductionmentioning

confidence: 99%

“…Arsenic (As), a potent environmental toxin, is present in both organic and inorganic forms as trivalent and pentavalent salts. It is used in the manufacturing of semiconductors, dyes, wood preservatives, glass, and agricultural pesticides 1 . This hazardous metal is considered as a potent environmental toxic agent, and chronic small‐dose arsenic exposure represents a major concern owing to its carcinogenic effects on human populations.…”

Section: Introductionmentioning

confidence: 99%

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Nephroprotective effects of chlorogenic acid against sodium arsenite‐induced oxidative stress, inflammation, and apoptosis

et al. 2020

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BACKGROUND: Chronic exposure to arsenic (As) leads to serious renal disorders. Chlorogenic acid (CGA), a phenolic compound, has several well known physiological benefits, including antioxidant and anti-inflammatory activities. The present study investigated the potential renoprotective effects of CGA on sodium arsenite (NaAsO 2)-induced kidney damage in mice. The mice were randomly allocated into five groups to receive daily treatment with CGA (200 mg kg −1), NaAsO 2 (5 mg kg −1), NaAsO 2 + CGA (100 mg kg −1), NaAsO 2 + CGA (200 mg kg −1), or a control for 28 days. RESULTS: In the NaAsO 2-treated group, NaAsO 2 induced significant renal dysfunction, oxidative damage, inflammation, and apoptosis, as demonstrated by marked increases in urea and creatinine levels accompanied by a decrease in the kidney index. Considerable increases in malondialdehyde and nitric oxide levels and parallel decreases in various antioxidant markers (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione) levels were also detected in the renal tissues of NaAsO 2-treated mice. NaAsO 2 exposure was associated with marked increases in renal inflammatory markers (interleukin-1⊎ and tumor necrosis factor-⊍) and apoptosis indicators including Bax and caspase-3 levels contaminant, with a marked decrease in Bcl-2, an anti-apoptotic protein, in the NaAsO 2-treated group compared with the control group. However, pretreatment with CGA substantially mitigated the renal injury and dysfunction associated with NaAsO 2 exposure by reducing tissue inflammation and apoptosis and improving the antioxidant status. The CGA pretreatment also alleviated the NaAsO 2induced histological alterations in renal tissues. CONCLUSION: Taken together, our results suggest the efficacy of CGA in alleviating As-mediated renal tissue damage.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Nephroprotective effects of chlorogenic acid against sodium arsenite‐induced oxidative stress, inflammation, and apoptosis

et al. 2020

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“…The generation of free radicals, reactive oxygen species (ROS), and reactive nitrogen species (RNS), leads to oxidative stress when their presence exceeds the antioxidant capacity of the cells to counterbalance their effects (Azab et al 2013, Mumtaz et al 2020. Almeer et al (2019a) stated that Cd enhances the production of free radicals as well as suppresses the scavenging system in cells, resulting in oxidative stress, lipid peroxidation, and apoptosis by disturbing mitochondrial function and redox metabolism.…”

Section: Introductionmentioning

confidence: 99%

Involvement of redox status and the nuclear-related factor 2 in protecting against cadmium-induced renal injury with Sana Makki (Cassia senna L.) pre-treatment in male rats

Albasher

Albrahim

Aljarba

et al. 2020

An. Acad. Bras. Ciênc.

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This study was designed to investigate the potential defensive strategy of Sana Makki extract (SME) against Cd-induced in vivo nephrotoxicity and its underlying mechanisms. Male albino rats were used in a thirty days study comparing control, SMEtreated, CdCl 2 -treated, and combined SME and Cd treatment. Pre-treatment with SME signifi cantly reduced serum kidney biomarkers (urea and creatinine), the concentration of renal KIM-1, and kidney index values. Additionally, SME also attenuated CdCl 2 -induced oxidative and nitrosative stress in renal tissue; signifi cantly reducing malondialdehyde (MDA) and nitric oxide (NO) concentrations and signifi cantly increasing antioxidant enzymes in kidney tissue. Molecularly, SME signifi cantly upregulated antioxidant gene expression (SOD2, GR, GPx1, and CAT) caused by Cd. Notably, the augmented mRNA expression of nuclear-related factor 2 (Nrf2) by Cd was enhanced by SME administration. SME markedly suppressed the Cd-induced rise in pro-infl ammatory cytokines. The combination of Cd and SME relieved the Cd-induced apoptotic damage by enhancing Bcl2 and suppressing Bax and Cas-3 levels in renal tissue. The renal tissue histoarchitecture confi rmed the biochemical and molecular fi ndings. Collectively, our data indicate that SME can counteract Cd-induced renal intoxication through anti-oxidative, antiinfl ammatory, and anti-apoptotic mechanisms.

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“…The inhibition of CAT and GSH-Px after Cd intoxication has been attributed to Fe and Se depletion that very important for CAT and GSH-Px functions, respectively 20 . Moreover, the inhibition of T-SOD could be due to the interaction between Cd and the protein part of SOD which causes alternation in the enzyme configuration, thus inhibiting its catalytic property 21 . It has been assumed that the antioxidants may alleviate Cd-induced oxidative stress due to their capacity to quench free radicals and enhance the activity of endogenous antioxidant defense enzymes 22 .…”

Section: Discussionmentioning

confidence: 99%

Zingerone alleviates cadmium-induced nephrotoxicity in rats via its antioxidant and anti-apoptotic properties

Dawood

Mumtaz

Padiya

2022

Rev. Ciênc. Farm. Básica Apl.

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Objectives: Cadmium is an essential industrial metal and acts as an environmental toxicant that is a major cause of kidney diseases. Hence, we aimed to evaluate the possible nephroprotective effects of zingerone (ZGO), a major flavonoid constituent in ginger (Zingiber officinale) dry roots, against cadmium-induced nephrotoxicity in rats. Methods: In this study, Wistar albino rats [ACUC: HU2020/Z/FMS0120-01] were allocated randomly to 4 groups with seven animals in each group. The control group which received physiological saline; cadmium chloride (CdCl 2 ) treatment group which received CdCl 2 at a dose of 6.5 mg/kg intraperitoneally (i.p.) for 7 consecutive days; zingerone treatment group which received 25 mg/kg of zingerone orally for 7 consecutive days and CdCl 2 (6.5 mg/kg; i.p.)+ZGO (25 mg/kg; p.o.) treatment group which received CdCl 2 and ZGO for 7 consecutive days. Results: Co-administration of ZGO along with CdCl 2 resulted in a significant reduction in creatinine and urea levels of serum. Additionally, ZGO significantly diminished the tissue levels of Cd concentration, lipid peroxidation, and nitric oxide and significantly recovered the enzymatic and nonenzymatic antioxidant molecules, namely glutathione, total superoxide dismutase, catalase, and glutathione recycling enzymes peroxidase and reductase, in kidney tissue. Furthermore, ZGO treatment prevented the inflammation produced by CdCl 2 by restraining the elevation in the level of pro-inflammatory cytokines (tumor necrosis factor-alpha and interleukin-1beta). Moreover, ZGO improved histopathological alternations in the kidney by preventing apoptosis cascade in kidney tissue by stimulating Bcl-2 and suppressing Bax and caspase-3. Conclusions: Our findings suggest that ZGO has nephroprotective activity in cadmium-induced nephrotoxicity mostly via modulating of oxidant/antioxidant balance, inflammatory response, and apoptosis.

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Exposure to arsenite and cadmium induces organotoxicity and miRNAs deregulation in male rats

Cited by 19 publications

References 60 publications

Nephroprotective effects of chlorogenic acid against sodium arsenite‐induced oxidative stress, inflammation, and apoptosis

Nephroprotective effects of chlorogenic acid against sodium arsenite‐induced oxidative stress, inflammation, and apoptosis

Involvement of redox status and the nuclear-related factor 2 in protecting against cadmium-induced renal injury with Sana Makki (Cassia senna L.) pre-treatment in male rats

Zingerone alleviates cadmium-induced nephrotoxicity in rats via its antioxidant and anti-apoptotic properties

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