Potential Toxicity of Plant Growth Regulator Gibberellic acid (GA3) on the Pancreatic Structures and Functions in the albino rat
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Jul-Dec 2016 | Vol 2 | Issue 2 | Page :11-26

Olfat A. Abd-El- Aty1, Rehab A. Masoud2

1Department of Anatomy, Faculty of Medicine for Girls, Al-Azhar University, Cairo, Egypt.
2Forensic medicine and clinical toxicology departments, Faculty of Medicine for Girls, Al-Azhar University, Cairo, Egypt.

How to cite this article::Abd-El- Aty OA, Masoud RA. Potential Toxicity of Plant Growth Regulator Gibberellic acid (GA3) on the Pancreatic Structures and Functions in the albino rat. Acad. Anat. Int. 2016;2(2):11-26.


Background: Gibberellic acid (GA3) affects many mechanisms of plant growth including stem elongation by stimulating rapid cell division and elongation, flowering, fruit development and breaking dormancy. GA3 is highly persistent and bioactive in soil for months. Since it is easily absorbed dermally, orally or by inhalation; it can injure liver, kidney, muscle and brain tissues. Aim of work: to explore the toxic effect induced by ingestion of residues of GA3 on the pancreas. Methods: Sixty male albino rats, were divided into four equal groups: Group I (negative control): received free water. Group II (positive control): received orally 30± 3ml of solution contained 1 N NaOH 5days/week for 6 weeks. Group III (Treated group): received orally daily 2.2± 0.3mg of GA3 5days/week for 6 weeks .Group IV (recovery group): take the same doses and period similar to group III and left without treatment for another 6 weeks. Fasting blood glucose levels were assessed two times per week to all rats during the experiment. At the end of the experimental period, Malondialdehyde (MDA), Superoxide dismutase (SOD) and Glutathione peroxidase (GSH-PX) and Catalase (CAT) were determined, in addition to serum amylase and lipase activity. Moreover, histological examination of the pancreatic tissue was carried by light and electron microscopes further-more, insulin immunohistochemical activity and morphometric study were done. Results: Ingestion of residues of GA3 for 6weeks cause significant elevation (P < 0.001) of MDA and significant drop (P < 0.001) of GSH-PX, SOD and CAT. By stoppage of GA3 lipid peroxidation profile didn't improve completely and still increased above the control levels. Also, GSH-PX and SOD and CAT still decreased significantly. Histological examination express cellular damage with degenerative changes in cells of islet of Langerhans in the form of less population of cells which contained vacuolated cytoplasm and deeply stained or pyknotic nuclei with presence of dilatation of the fenestrated capillary. Ultra structural results of the acinar cells showed irregular contours of nuclei, dilated irregular rough endoplasmic reticulum and reduction of the quantity of the secretory granules with presence of multiple cytoplasmic vacuolations in addition to presence of auotophagic vacuoles. Insulin immunohistochemical staining of islets showing small, atrophied andnegative insulin-immunoreactive spots. The morphometric results represent significant reduction (P < 0.001) in the number of islets/pancreas sections and the number of beta cells/islet. The insult which denoted didn't resolve completely by the 6 week recovery period which may suspect the occurrence of chronic pancreatitis due to oxidative stress. Conclusion: Residual doses of GA3 exposed the pancreases to oxidative stress and 6 weeks is not enough to complete full recovery.

Keywords:GA3, Pancreases, oxidative stress, Ultrastructure, Insulin immunohistochemistry, morphometric study.

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