Curcumin prevents Cr(VI)-induced renal oxidant damage by a mitochondrial pathway

Molina‐Jijón, Eduardo; Tapia, Edilia; Zazueta, Cecilia; Hafidi, Mohammed El; Zatarain-Barrón, Zyanya Lucía; Hernández-Pando, Rogelio; Medina-Campos, Omar Noel; Zarco-Márquez, Guillermo; Torres, Ignacio; Pedraza‐Chaverrí, José

doi:10.1016/j.freeradbiomed.2011.07.018

Cited by 152 publications

(138 citation statements)

References 94 publications

Supporting

Mentioning

130

Contrasting

Order By: Relevance

“…Because of that, attention has been focused on the toxic action of Cr(VI), since it is highly hepatotoxic (Rafael et al, 2007) and nephrotoxic (Khan et al, 2010;Molina-Jijón et al, 2011). Moreover, certain studies have indicated that this metal accumulates in the liver and kidneys (Sutherland et al, 2000;O'Brien et al, 2003;Collins et al, 2010;Chang et al, 2011), corroborating the results found here.…”

Section: Discussionsupporting

confidence: 87%

“…Published reports have shown that the use of natural products rich in antioxidants, such as polyphenols, can reduce the toxic effects of Cr(VI) (Arreola-Mendoza et al, 2006;Kalayarasan et al, 2008;Pedraza-Chaverri et al, 2008;Guha et al, 2010;Khan et al, 2010;Molina-Jijón et al, 2011;Deb et al, 2012). Thus, the chemoprotective effect demonstrated here may be related, at least in part, to the reduction of Cr(VI)-induced oxidative stress, since pomegranate contains polyphenols with antioxidant properties, such as punicalin and punicalagin, its main metabolites.…”

Section: Discussionmentioning

confidence: 67%

See 1 more Smart Citation

Punica granatum L. protects mice against hexavalent chromium-induced genotoxicity

Ávila

Guerra

Borges

et al. 2013

Braz. J. Pharm. Sci.

View full text Add to dashboard Cite

This study investigated the chemoprotective effects of Punica granatum L. (Punicaceae) fruits alcoholic extract (PGE) on mice exposed to hexavalent chromium [Cr(VI)]. Animals were pretreated with PGE (25, 50 or 75 mg/kg/day) for 10 days and subsequently exposed to a sub-lethal dose of Cr(VI) (30 mg/kg). The frequency of micronucleated polychromatic erythrocytes in the bone marrow was investigated and the Cr(VI) levels were measured in the kidneys, liver and plasm. For the survival analysis, mice were previously treated with PGE for 10 days and exposed to a single lethal dose of Cr(VI) (50 mg/kg). Exposure to a sub-lethal dose of Cr(VI) induced a significant increase in the frequency of micronucleated cells. However, the prophylactic treatment with PGE led to a reduction of 44.5% (25 mg/kg), 86.3% (50 mg/kg) and 64.2% (75 mg/kg) in the incidence of micronuclei. In addition, the 50 mg/kg dose of PGE produced a higher chemoprotective effect, since the survival rate was 90%, when compared to that of the non-treated group. In these animals, reduced amounts of chromium were detected in the biological materials, in comparison with the other groups. Taken together, the results demonstrated that PGE exerts a protective effect against Cr(VI)-induced genotoxicity. Uniterms INTRODUCTIONChromium occurs naturally in the environment in different oxidation states, where Cr(III) and Cr(VI) are the most prevalent. The hexavalent form is usually linked with oxygen and is a strong oxidizing agent. Studies have shown that Cr(VI) is a mutagenic, carcinogenic and teratogenic agent, which easily penetrates the cell membrane in the form of chromate anion (Barceloux, 1999;Acharya et al., 2006;Nickens et al., 2010;Chang et al., 2011;Okello et al., 2012). Its molecular mechanisms of toxicity are not yet fully known, but it is believed that the intracellular increase in the production of reactive oxygen species (ROS) is probably a key factor in inducing cell damage (Ye et al., 1999;Wu et al., 2012). These reactive species can cause damage to macromolecules such as DNA, proteins and lipids, thereby inhibiting their functions (Valko et al., 2007;Yan et al., 2012) and may even trigger apoptotic cell death (Liu, Chen, 2006;Liu et al., 2008).Cr(VI) has been widely used in metallurgical, refractory and chemical industries. It has been considered a potent occupational carcinogen among workers involved in electrodeposition, metal finishes/welding, wood preservatives, organic synthesis procedures and in leather tanning (Barceloux, 1999;Shrivastava et al., 2002;Acharya et al., 2006;Nickens et al., 2010). In such activities occupational exposure to Cr(VI)-contaminated dust and aerosols occurs predominantly through inhalation or skin contact (Zagrodzki et al., 2007). Non-occupational exposure to Cr(VI) can also occur through cigarette smoke, automobile emissions and the inappropriate disposal of chromium-containing waste in the environment (O'Brien et al., 2003;Russo et al., 2005).The literature has shown that the administration of antioxidant agents ...

show abstract

Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 67%

Punica granatum L. protects mice against hexavalent chromium-induced genotoxicity

Ávila

Guerra

Borges

et al. 2013

Braz. J. Pharm. Sci.

View full text Add to dashboard Cite

show abstract

“…In contrast natural phytochemical Nrf2 activators such as sulforaphane, epigallocatechin-3-gallate, and curcumin, improve nephropathy in animal models of acute or chronic kidney diseases of diverse etiologies [19][20][21][22][23]. Together these observations support the role of Nrf2 deficiency in the pathogenesis of oxidative stress, inflammation, and progression of kidney disease.…”

Section: Introductionmentioning

confidence: 64%

“…Activation of these pathways confers protection by up-regulating expression of antioxidant enzymes, detoxifying compounds, protein chaperones, and trophic factors. In fact these phytochemicals have been shown to prevent or ameliorate a variety of diseases including cardiovascular disease [42,43], neurodegenerative disorders [44][45][46][47][48][49], and acute and chronic kidney disease [19][20][21][22][23]. In contrast, excessive or unrestrained activity of Nrf2 system has been shown to have adverse consequences.…”

Section: Discussionmentioning

confidence: 99%

Dose-dependent deleterious and salutary actions of the Nrf2 inducer dh404 in chronic kidney disease

Vaziri¹,

Liu²,

Farzaneh³

et al. 2015

Free Radical Biology and Medicine

View full text Add to dashboard Cite

Oxidative stress and inflammation play a central role in progression and complications of CKD and are, in part, due to impairment of the Nrf2 system which regulates expression of antioxidant and detoxifying molecules. Natural Nrf2 inducing phytochemicals have been shown to ameliorate kidney disease in experimental animals. However due to adverse outcomes clinical trial of synthetic Nrf2 activator, bardoxolone methyl (BARD), in CKD patients was terminated. BARD activates Nrf2 via 2 covalent modification of reactive cysteine residues in Nrf2 repressor molecule, Keap-1. In addition to Nrf2, Keap1 suppresses IKKB, the positive regulator of NF k B. Treatment with BARD analog, dh404, at 5-20 mg/kg/day in diabetic obese Zucker rats exacerbates whereas its use at 2 mg/kg/day in 5/6 nephrectomized rats attenuates CKD progression. We, therefore, hypothesized that deleterious effects of high dose BARD are mediated by activation of NF k B.CKD (5/6 nephrectomized) rats were randomized to receive dh404 (2 or 10mg/kg/day) or vehicle for 12 weeks. Vehicle-treated group exhibited glomerulosclerosis, interstitial fibrosis and inflammation, activation of NF k B, upregulation of oxidative, inflammatory and fibrotic pathways, and suppression of Nrf2 activity and its key target gene products. Treatment with low dose dh404 restored Nrf2 activity and expression of its target genes, attenuated activation of NF k B and fibrotic pathways, and reduced glomerulosclerosis, interstitial fibrosis and inflammation. In contrast treatment with high dh404 dosage intensified proteinuria, renal dysfunction and histological abnormalities, amplified up-regulations of NF k B and fibrotic pathways, and suppression of Nrf2 system. Thus therapy with BARD analogs exerts a dose-dependent dimorphic impact on CKD progression.

show abstract

“…The level of catalase was significantly (p<0.05) decreased in Cr-treated birds compared to control group in the present study. Previous studies noted depression in catalase following Cr-administration in rats (Molina-Jijon et al, 2011) and fish (Shaheen and Akhtar, 2012). The first line of defense of antioxidant enzyme system is superoxide dismutase then comes the catalase.…”

Section: Discussionmentioning

confidence: 81%

Chromium Toxicity and Oxidative Stress in Broiler Chicks and its Amelioration with Vitamin E and Bentonite

Mashkoor¹,

Khan²,

Khan³

et al. 2016

IJAB

View full text Add to dashboard Cite

This experiment utilized 140 one-day-old broiler chickens. Group 1 served as control. Birds of groups 2, 5, 6 and 7 were administered chromium (Potassium dichromate, K2Cr2O7; Cr 6+ ) @ 270 mg/kg through the feed. Groups 3, 5 and 7 received vitamin E (150 mg/kg) and groups 4, 6 and 7 received bentonite (5% of feed), respectively. Cr-treated birds were dull and depressed and gained significantly less body weight gain and increased feed conversion ratio (FCR). All the birds treated with Cr (group 2) showed a significant decrease in hematological parameters at day 21 and 42. Biochemical parameters i.e. total protein, albumin and globulin were decreased while ALT, AST, urea and creatinie were increased at day 21 and 42. Birds treated with Cr (group 2) showed a significant decrease in total antioxidant activity and catalase, while malondialdehyde (MDA) and total oxidant status levels were increased at days 21 and 42. Co-administration of bentonite along with Cr resulted in partial amelioration (group 6) as compared to groups 5 and 7 administered chromium + vitamin E and chromium + vitamin E + bentonite, respectively. Highest concentration of Cr was determined in Cr treated birds (group 2) followed by groups 2, 6, 5 and 7 at 21 and 42 experimental days. It was concluded that Cr leads to oxidative stress in broilers. Vitamin E and bentonite partially ameliorated Cr toxicity. The combination of vitamin E and bentonite is promising in combating Cr toxicity effects.

show abstract

Curcumin prevents Cr(VI)-induced renal oxidant damage by a mitochondrial pathway

Cited by 152 publications

References 94 publications

Punica granatum L. protects mice against hexavalent chromium-induced genotoxicity

Punica granatum L. protects mice against hexavalent chromium-induced genotoxicity

Dose-dependent deleterious and salutary actions of the Nrf2 inducer dh404 in chronic kidney disease

Chromium Toxicity and Oxidative Stress in Broiler Chicks and its Amelioration with Vitamin E and Bentonite

Contact Info

Product

Resources

About