Evaluation of Lead Hepatotoxicity; Histological, Histochemical and Ultrastructural Study
• 2014
معلومات البحث
المؤلفون
Ahmed M. S. Hegazy, Usama A. Fouad
الكلمات المفتاحية
Lead, Rats, Liver, Light Microscope, Electron Microscope
المجلة العلمية
Not Available
الناشر
Not Available
المجلد
Not Available
العدد
Not Available
الصفحات
Not Available
publication.type
International
رابط البحث
Not Available
المواد المرفقة
Not Available
الملخص
Lead is one of the most well-known naturally occurring environmental heavy metals. This experimental
study was designed to evaluate lead induced toxic effects on hepatocytes and lobular architecture
as judged microscopically. Material and Methods: This study was conducted in anatomy
department, Benha faculty of medicine, Benha University, Egypt from May to October 2013 on 30
normal adult albino rats divided into 3 groups; one control and 2 experimental groups. The experimental
groups were given 0.13% lead acetate solution in drinking water for 4 and 8 weeks, respectively.
Animals were scarified and livers were removed and used to identify microscopic changes.
Specimens were stained with Hematoxylin and eosin, with Masson trichrome stain for study
of fibrous tissue and with periodic acid shiff's (PAS) to study the glycogen content .Other specimens
were prepared for ultrastructural study. Results: Mild lymphocytic infiltration, vacuolar
degeneration and mild increase of periportal fibrosis with mild depletion of glycogen content and
partial disappearance of glycogen vacuoles were reported in animals received contaminated
water for 4 weeks. Animals maintained for 8 weeks on contaminated water showed hepatic changes
in the form of abundant lymphocytic infiltration, increased cellular polymorphism, pyknotic
nuclei and areas of cell necrosis with evident moderate periportal fibrosis and marked
vacuolar degeneration associated with marked depletion of glycogen content. Ultrastructural
study revealed mitochondrial edema, appearance of interstitial inflammatory cells, and appearance
of scattered variable sized lead electron-dense inclusion bodies. Conclusion: It could be concluded
that chronic exposure to lead imposes a potent toxic effect on liver cells manifested as glycogen
depletion, cellular infiltration and liver architecture in the form of initiation of periportal
fibrosis that may progress to liver cirrhosis.
study was designed to evaluate lead induced toxic effects on hepatocytes and lobular architecture
as judged microscopically. Material and Methods: This study was conducted in anatomy
department, Benha faculty of medicine, Benha University, Egypt from May to October 2013 on 30
normal adult albino rats divided into 3 groups; one control and 2 experimental groups. The experimental
groups were given 0.13% lead acetate solution in drinking water for 4 and 8 weeks, respectively.
Animals were scarified and livers were removed and used to identify microscopic changes.
Specimens were stained with Hematoxylin and eosin, with Masson trichrome stain for study
of fibrous tissue and with periodic acid shiff's (PAS) to study the glycogen content .Other specimens
were prepared for ultrastructural study. Results: Mild lymphocytic infiltration, vacuolar
degeneration and mild increase of periportal fibrosis with mild depletion of glycogen content and
partial disappearance of glycogen vacuoles were reported in animals received contaminated
water for 4 weeks. Animals maintained for 8 weeks on contaminated water showed hepatic changes
in the form of abundant lymphocytic infiltration, increased cellular polymorphism, pyknotic
nuclei and areas of cell necrosis with evident moderate periportal fibrosis and marked
vacuolar degeneration associated with marked depletion of glycogen content. Ultrastructural
study revealed mitochondrial edema, appearance of interstitial inflammatory cells, and appearance
of scattered variable sized lead electron-dense inclusion bodies. Conclusion: It could be concluded
that chronic exposure to lead imposes a potent toxic effect on liver cells manifested as glycogen
depletion, cellular infiltration and liver architecture in the form of initiation of periportal
fibrosis that may progress to liver cirrhosis.
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