Curcumin Attenuates Hepatotoxicity Induced by Zinc Oxide Nanoparticles in Rats

Khorsandi, Layasadat; Mansouri, Esrafil; Orazizadeh, Mahmoud; Jozi, Zahra

doi:10.5152/balkanmedj.2016.150017

Cited by 20 publications

(8 citation statements)

References 24 publications

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“…In the high dosetreated rats, Zn concentration of kidney was significantly more than control while histopathological alterations were not observed in the kidney of this animals. Thus, (34). Interestingly, oxidative stress and apoptosis can be induced by ZNP in vitro (35).…”

Section: Discussionmentioning

confidence: 99%

Nephrotoxic effects of low-dose zinc oxide nanoparticles in rats

Khorsandi¹,

Moghadam²,

Jozi³

2018

J Nephropathol

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Background: The use of zinc oxide nanoparticles (ZNPs) in various products such as biosensors, sunscreens and nourishment added substances is increasing. Objectives: In the present work the impacts of ZNP on kidney of rats was explored. Materials and Methods: In this experimental study male Wistar rats were used. Trial groups received 5, 50 and 300 mg/kg ZNP (ZNP-1 to ZNP-3) for 2 weeks. Control group received only normal saline. blood urea nitrogen (BUN), creatinine (Cr) and uric acid were considered as biomarkers to indicate nephrotoxicity. To evaluate the oxidative stress in the kidney, malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPx) enzymes activity were measured. Histopathological and apoptotic cell death was also evaluated in renal tissues.Results: Blood density of zinc (Zn) was significantly increased in the low dose-treated rats. Concentration of Zn in the renal tissue was significantly increased in the high dose treated rats. Weight of kidney was significantly elevated in both ZNP-1 and ZNP-2 groups. ZNP resulted in a significant increment in MDA content in the low measurements and a critical reduction in the activity of the SOD and GPx enzymes. Exposure of ZNP at low dose induced a significant elevation in blood concentration of BUN, Cr and uric acid. Treatment with low dose of ZNP caused a significant increase in histological changes and apoptotic index. ZNP at the high dose induced poor nephrotoxicity. Conclusion: In conclusion, ZNP has dose-dependent nephrotoxic effects on rats and lower doses have more toxic action. ABSTRACT Implication for health policy/practice/research/medical education:In this study we demonstrated that zinc oxide nanoparticles (ZNPs) dose-dependently induced nephrotoxicity by elevation blood biochemical markers and generation of stress oxidative. ZNPs dose-dependently induced structural changes and increased apoptosis in renal tissue. Lower doses of this nanoparticle have more nephrotoxicity effects. The results of this study highlighted the requirement for alert during the utilization of ZNPs to prevent health impacts. Please cite this paper as: Khorsandi L, Heidari-Moghadam A, Jozi Z. Nephrotoxic effects of low-dose zinc oxide nanoparticles in rats. J Nephropathol. 2018;7(3):158-165.

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Section: Discussionmentioning

confidence: 99%

Nephrotoxic effects of low-dose zinc oxide nanoparticles in rats

Khorsandi¹,

Moghadam²,

Jozi³

2018

J Nephropathol

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“…Due to the accumulation of nanoparticles in different organs of experimental animals, including liver, spleen, brain and so forth, administration of NZnO (50 mg/kg/day) and treatment with curcumin (200 mg/kg/day) were measured in rats exposed to hepatotoxicity. The increased serum ALT, AST and ALP activity and MDA, decreased GPx and SOD levels suggests a link between NZnO and hepatic oxidative stress [ 111 ]. Although sodium fluoride is a substance that induces toxicity and oxidative stress, Moghaddam et al showed that the protective effect of curcumin was related to its ability to adjust the imbalance of antioxidant enzymes and reduced lipid peroxidation levels in rat with fluoride-induced hepatotoxicity [ 112 ].…”

Section: Cellular and Molecular Mechanisms Of Curcumin In The Prevmentioning

confidence: 99%

Curcumin in Liver Diseases: A Systematic Review of the Cellular Mechanisms of Oxidative Stress and Clinical Perspective

et al. 2018

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Oxidative stress has been considered a key causing factor of liver damage induced by a variety of agents, including alcohol, drugs, viral infections, environmental pollutants and dietary components, which in turn results in progression of liver injury, non-alcoholic steatohepatitis, non-alcoholic liver disease, liver fibrosis and cirrhosis. During the past 30 years and even after the major progress in the liver disease management, millions of people worldwide still suffer from an acute or chronic liver condition. Curcumin is one of the most commonly used indigenous molecules endowed by various shielding functionalities that protects the liver. The aim of the present study is to comprehensively review pharmacological effects and molecular mechanisms, as well as clinical evidence, of curcumin as a lead compound in the prevention and treatment of oxidative associated liver diseases. For this purpose, electronic databases including “Scopus,” “PubMed,” “Science Direct” and “Cochrane library” were extensively searched with the keywords “curcumin or curcuminoids” and “hepatoprotective or hepatotoxicity or liver” along with “oxidative or oxidant.” Results showed that curcumin exerts remarkable protective and therapeutic effects of oxidative associated liver diseases through various cellular and molecular mechanisms. Those mechanisms include suppressing the proinflammatory cytokines, lipid perodixation products, PI3K/Akt and hepatic stellate cells activation, as well as ameliorating cellular responses to oxidative stress such as the expression of Nrf2, SOD, CAT, GSH, GPx and GR. Taking together, curcumin itself acts as a free radical scavenger over the activity of different kinds of ROS via its phenolic, β-diketone and methoxy group. Further clinical studies are still needed in order to recognize the structure-activity relationships and molecular mechanisms of curcumin in oxidative associated liver diseases.

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“…bwt showed severe microvesicularsteatosis; accumulation of small lipid droplets in hepatocytes cytoplasm.Such finding is completely goes hand in hand withthe description of Khorsandi etal., [23] who clarified that lobular structures of the liver were damaged in NZnO-intoxicated rats. Centrilobular hepatocytes showed microvesicularsteatosis, accumulation of erythrocytes in central vein and sinusoids and infltration of infammatory cells were also observed.…”

Section: Discussionmentioning

confidence: 99%

Histological Changes of MaleWestarRats liver Following the Ingestion of Zinc Oxide Nanoparticles With special Emphasis on the Histochemical Alterations

Alferah¹

2018

J Histol Histopathol

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The present investigation was carried out on forty apparently healthy mature male Westar rats weighing between 120-200 gm with average three months age. The rats wereobtained from laboratory animal unite in the faculty of pharmacy, King Saud University and were divided randomly into four groups (10 rats/ group). Group I (G1) was kept as a control, Group II (G2)was obtained ZnO NPsin a dose 100 mg/kg body weight, Group III(G3) was obtained ZnO NPsin a dose 250 mg/kg BW, Group IV(G4) was obtained ZnO NPsin a dose 500 mg/kg BW and all treated groups received ZnO NPs by oral gavage for 21 days. G1 showed normal histological structure of all hepatic tissues without any abnormalities. G2 and G3 showed mild to moderate steatosis, necrosis with focal scattered of infammatory cells infltration with fibrous tissue proliferation and moderate hepatocytes glycogen depletion. Meanwhile, G4 showed severe steatosis, diffuse degeneration of hepatic tissues with loss of the hepatic architectures, sever fibrous tissue proliferation with anti-inflammatory cells infiltration as well as severe congestion with the hepatic artery, sinusoids and Portal vein. In addition, sever sinusoidal dilatation accompanied by Kupffer cells hyperplasia in between the hepatic cords were clarified. Furthermore, with PAS stain, sever hepatocytes glycogen depletion were claimed. The present investigation was concluded that the ZnO NPs have potential oxidative stress in the hepatic tissues that may affect the function of the liver.

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Curcumin Attenuates Hepatotoxicity Induced by Zinc Oxide Nanoparticles in Rats

Cited by 20 publications

References 24 publications

Nephrotoxic effects of low-dose zinc oxide nanoparticles in rats

Nephrotoxic effects of low-dose zinc oxide nanoparticles in rats

Curcumin in Liver Diseases: A Systematic Review of the Cellular Mechanisms of Oxidative Stress and Clinical Perspective

Histological Changes of MaleWestarRats liver Following the Ingestion of Zinc Oxide Nanoparticles With special Emphasis on the Histochemical Alterations

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