Zinc oxide nanoparticles hepatotoxicity: Histological and histochemical study

Al‐Μansour, Mubarak; Alferah, Mosaid A.; Shraideh, Z.; Jarrar, Bashir M.

doi:10.1016/j.etap.2017.02.015

Cited by 75 publications

(38 citation statements)

References 41 publications

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“…These findings are in agreement with the results of Almansour et al, [27] who showed that the liver of ZnO NPs treated rats exhibited sinusoidal dilatation accompanied by Kupffer cells activation and enlarged that lining the walls of sinusoids. This abnormality was also demonstrated in the toluidine blue stained semi thin sections.…”

Section: Discussionsupporting

confidence: 93%

“…Hepatocytes necrotic changes were evident; a small, pyknotic cellular nuclei with condensed chromatin, lack of nucleolus and acidophilic cytoplasm were observed were recognized. These results are in parallelism with the result of Almansour et al, [27] who observed that the liver of ZnO NPs treated rats for 21 days demonstrated well-defined necrotic hepatocytes. And also, hepatocytes cyto- plasmic vacuolation with partial cytoplasmic swelling was well demonstrated.…”

Section: Discussionsupporting

confidence: 91%

“…These investigations are in coincidence with the description of Almansour et al, [27] who observed that PAS stain exhibited partial hepatocytes glycogen content depletion. The later, was mainly observed in the degenerative hepatocytes.…”

Section: Discussionsupporting

confidence: 91%

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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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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 91%

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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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“…Since the size of the particles is less than 100 nm, they are on the same scale as many biological molecules. There is, therefore, a great need to better understand the interactions of nanoparticles with the liver from the organ to cell perspective [66].…”

Section: Tem Analysis Of Liver and Kidney Biopsiesmentioning

confidence: 99%

Controlled synthesis of ZnO nanoparticles and evaluation of their toxicity in Mus musculus mice

et al. 2018

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Zinc oxide nanoparticles (ZnO-NPs) of different sizes and morphology were synthesized. The variables analyzed were zinc precursor concentration, the nature of the synthesis solvent and the concentration of surfactant agent. The solids synthesized were characterized using IR spectroscopy, X-ray diffraction (XRD) and transmission electron microscopy (TEM). Considering the nature of the synthesis process, a tentative model of the mechanism of formation of the ZnO-NPs was proposed. ZnO-NPs with spheroidal morphology were obtained with a 10 mM CTAB concentration and these were selected to study their toxicity. For this study, Mus musculus mice were therefore given an oral dose of 50 mg ZnO/kg body weight (b.v.). Biopsies obtained from the livers and kidneys of the mice studied were analyzed using TEM and atomic absorption. The biopsy of the liver of the mouse given a dose of ZnO-NPs showed evidence of steatosis. The atomic absorption results showed the accumulation of Zn in both the liver and the kidney of the mouse.

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“…Exposure to zinc oxide (ZnO)‐NPs is reported to induce hepatotoxicity in mice and rats represented by several morphological and cellular damage signs in liver tissue, including focal necrosis, ER swelling, increase in liver enzyme levels, upregulation of stress‐related genes and depletion in GSH. Histological and histochemical alterations have been observed in rat tissue, comprising cellular destruction and deprivation (Almansour, Alferah, Shraideh, & Jarrar, ). Yang et al () concluded their observations that the occurrence of apoptotic cell death is mediated via caspase‐3, ‐9 and ‐12, and JNK phosphorylation, in addition to elevated pro‐apoptotic Bax protein (Yang et al, ).…”

Section: Means Of Chemical Modulation Of Hepatic Apoptosismentioning

confidence: 99%

Chemical induction of hepatic apoptosis in rodents

Qinna

Ghanim

2018

J of Applied Toxicology

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The urge of identifying new pharmacological interventions to prevent or attenuate liver injury is of critical importance and needs an expanded experimental toolbox. Hepatocyte injury and cellular death is a prominent feature behind the pathology of liver diseases. Several research activities focused on identifying chemicals and hepatotoxicants that induce cell death by apoptosis, in addition to presenting its corresponding signaling pathway. Although such efforts provided further understanding of the mechanisms of cell death, it has also raised confusion concerning identifying the involvement of several modes of cell death including apoptosis, necrosis and fibrosis. The current review highlights the ability of several chemicals and potential hepatotoxicants to induce liver damage in rodents by means of apoptosis while the probable involvement of other modes of cell death is also exposed. Thus, several chemical substances including hepatotoxins, mycotoxins, hyperglycemia inducers, metallic nanoparticles and immunosuppressant drugs are reviewed to explore the hepatic cytotoxic spectrum they could exert on hepatocytes of rodents. In addition, the current review address the mechanism by which hepatotoxicity is initiated in hepatocytes in different rodents aiding the researcher in choosing the right animal model for a better research outcome.

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Zinc oxide nanoparticles hepatotoxicity: Histological and histochemical study

Cited by 75 publications

References 41 publications

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

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

Controlled synthesis of ZnO nanoparticles and evaluation of their toxicity in Mus musculus mice

Chemical induction of hepatic apoptosis in rodents

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