Nephroprotective action of tocotrienol-rich fraction (TRF) from palm oil against potassium dichromate (K2Cr2O7)-induced acute renal injury in rats

Khan, Mohd Rashid; Siddiqui, Shahla; Parveen, Kehkashan; Javed, Saleem; Diwakar, Sandhya; Siddiqui, Waseem Ahmad

doi:10.1016/j.cbi.2010.04.025

Cited by 41 publications

(37 citation statements)

References 45 publications

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“…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.

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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 ...

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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

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“…In addition, it can protect the depression of SOD activity (Augusti et al, 2008). Khan et al, (2010) provide evidence that potassium dichromate administration caused nephrotoxicity in both proximal tubule and glomerulus through OS induction. Tocotrienol, a member of vitamin E family, supplementation exhibited the capacity to reduce proximal tubular injury and renal LPO, and increased GSH level and catalase activity.…”

Section: Protective Effect Of Medicinal Plants-derived Antioxidants Imentioning

confidence: 97%

A review of oxidative stress in acute kidney injury: protective role of medicinal plants-derived antioxidants

Palipoch

2013

Afr. J. Trad. Compl. Alt. Med.

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Acute kidney injury (AKI) is the common clinical syndrome which is associated with increased morbidity and mortality. The severity extends from less to more advanced spectrums which link to biological, physical and chemical agents. Oxidative stress (OS)-related AKI has demonstrated the increasing of reactive oxygen species (ROS) and reactive nitrogen species (RNS) and the decreasing of endogenous antioxidants. Medicinal plants-derived antioxidants can be ameliorated oxidative stress-related AKI through reduction of lipid peroxidation (LPO) and enhancement of activities and levels of endogenous antioxidants. Therefore, medicinal plants are good sources of exogenous antioxidants which might be considered the important remedies to ameliorate pathological alterations in oxidative stress-related AKI.

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“…It is noteworthy that the radioprotective action of GT3 against vascular injury is mediated through a HMG-CoA reductase-dependent mechanism (Berbée et al, 2011). Chronic treatment of rats with a tocotrienol-rich fraction from palm oil decreases K 2 Cr 2 O 7 -induced kidney injury by decreasing morphological damage to renal proximal tubules and improving renal proximal tubular function, glomerular filtration rate, and cellular redox status (Khan et al, 2010). However, it is unknown which component of the tocotrienol-rich fraction is responsible for renal protection against K 2 Cr 2 O 7 -induced toxicity.…”

Section: Introductionmentioning

confidence: 99%

γ-Tocotrienol Protects against Mitochondrial Dysfunction and Renal Cell Death

Nowak¹,

Bakajsova²,

Hayes³

et al. 2011

J Pharmacol Exp Ther

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Oxidative stress is a major mechanism of a variety of renal diseases. Tocopherols and tocotrienols are well known antioxidants. This study aimed to determine whether ␥-tocotrienol (GT3) protects against mitochondrial dysfunction and renal proximal tubular cell (RPTC) injury caused by oxidants. Primary cultures of RPTCs were injured by using tert-butyl hydroperoxide (TBHP) in the absence and presence of GT3 or ␣-tocopherol (AT). Reactive oxygen species (ROS) production increased 300% in TBHP-injured RPTCs. State 3 respiration, oligomycinsensitive respiration, and respiratory control ratio (RCR) decreased 50, 63, and 47%, respectively. The number of RPTCs with polarized mitochondria decreased 54%. F 0 F 1 -ATPase activity and ATP content decreased 31 and 65%, respectively. Cell lysis increased from 3% in controls to 26 and 52% at 4 and 24 h, respectively, after TBHP exposure. GT3 blocked ROS production, ameliorated decreases in state 3 and oligomycinsensitive respirations and F 0 F 1 -ATPase activity, and maintained RCR and mitochondrial membrane potential (⌬⌿ m ) in injured RPTCs. GT3 maintained ATP content, blocked RPTC lysis at 4 h, and reduced it to 13% at 24 h after injury. Treatment with equivalent concentrations of AT did not block ROS production and cell lysis and moderately improved mitochondrial respiration and coupling. This is the first report demonstrating the protective effects of GT3 against RPTC injury by: 1) decreasing production of ROS, 2) improving mitochondrial respiration, coupling, ⌬⌿ m , and F 0 F 1 -ATPase function, 3) maintaining ATP levels, and 4) preventing RPTC lysis. Our data suggest that GT3 is superior to AT in protecting RPTCs against oxidant injury and may prove therapeutically valuable for preventing renal injury associated with oxidative stress.

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Nephroprotective action of tocotrienol-rich fraction (TRF) from palm oil against potassium dichromate (K2Cr2O7)-induced acute renal injury in rats

Cited by 41 publications

References 45 publications

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

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

A review of oxidative stress in acute kidney injury: protective role of medicinal plants-derived antioxidants

γ-Tocotrienol Protects against Mitochondrial Dysfunction and Renal Cell Death

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