In this study, most of the acinar cells had a few electron-dense secretory granules and many electron-lucent vacuoles. A few acinar cells had secretory granules with an electron-dense core surrounded by a moderate electron-dense zone. A few acinar cells had extremely rarified electron-lucent areas of cytoplasm that were nearly devoid of organelles. Most of the acinar cells had a dilated and fragmented RER. The mechanism of this cellular damage caused by aflatoxin B1 has not been fully elucidated. Some researchers have stated that the mechanism of action of aflatoxins on the cell was mediated through the production of free radicals and the oxidized products of oxidative stress such as ROS [22,23]. These ROS of oxidative stress are capable of alteration and damaging cellular lipid membranes, especially highly unsaturated fatty acids, through lipid peroxidation, leading to inhibition of protein synthesis and fragility of the zymogen granules [24,25]. The degenerative changes of the acini in this study were similar to those previously observed in chronic pancreatitis  and were in agreement with the results obtained by previous investigators  who attributed the presence of vacuoles in the quail's exocrine pancreas during aflatoxicosis to defective formation of zymogen granules.
In this study, biochemical analysis of serum amylase in the rats that received aflatoxin (group II) revealed a highly significant increase compared with control rats. These results confirm the acinar degenerative changes that were previously detected. The serum amylase enzyme level was observed to decrease within the first few hours after dimethoate intoxication, which might reflect an impairment of its synthesis by pancreatic acinar cells. Twenty-four hours after intoxication, a steady rise in the amylase enzyme level was observed .
In this study, some acinar cells had small condensed heterochromatic nuclei or irregular nuclei with peripheral heterochromatin condensation. Aflatoxin had an impact on the antioxidant defense system; therefore, it led to a marked increase in nitric oxide level. The nitric oxide product reacts with superoxides to produce high peroxynitrite anion toxicity. This toxicity could decrease mitochondrial respiration, deplete cellular glutathione, and damage DNA. Finally, proapoptotic effects in the form of small dark nuclei and condensation of the cytoplasm were induced [28,29].
The current research revealed vascular changes in the form of congested blood vessels. Jakhar and Sadana  observed varying degrees of congestion produced by aflatoxin B1 in many organs of quails, such as pancreas, skeletal muscles, myocardium, spleen, and lungs.
In this study, examinations of pancreas in the aflatoxin-received group revealed pancreatic lobules separated by thick interlobular septa with many collagen fibers especially around dilated ducts and blood vessels. Bundles of collagen fibers were seen between acini. The exposure to aflatoxin B1 results in an increase in fibrous tissue in the liver . Vitamin A-storing cells known as stellate cells were famous of being present in the liver . Stellate cells have also been observed in both rat and human pancreas and have been found to play a role in the development of pancreatic fibrosis . The inactive pancreatic stellate cells are triangular, lipid-containing cells predominantly located in perivascular regions. When activated, they lose their lipid droplets and take on a fibroblast-like morphologic appearance, become capable of synthesizing collagen types I, II, and fibronectin, and migrate to periacinar areas . This synthesis of collagen by stellate cells is initiated either by oxidative stress  or by complex release of multiple cytokines interleukin-1, interleukin-6, and transforming growth factor-α from a chronic cellular infiltration [25,36]. Therefore, it could be suggested that interstitial fibrosis was a key factor in the distortion of the histoarchitecture of both exocrine and endocrine pancreas .
In this study, mononuclear cellular infiltration and mast cells were detected between acini and close to islets of Langerhans in the aflatoxin-received group. These observations were in accordance with the results obtained by other researchers [26,38]. Aflatoxin ingestion leads to ROS production, which indirectly regulates chemokine receptor expression and some function of polymorphonuclear leukocytes (PMNLs). It also facilitates the recruitment and localization of polymorphonuclear leukocyte to the site of infection and inflammation . It was recorded that, during pancreatitis, inflammatory cells trigger the activation of signaling pathways regulating gene expression of inflammatory mediators or results in the increased production of cytokines, which leads to the progression of local pancreatic inflammation [39,40]. Dib et al.  found that mast cells potentially play a central role in the initiation of the inflammatory response, including increased vascular permeability and leukocyte accumulation. Lopez Font et al.  added that mast cell degranulation plays a pivotal role in the activation of leukocytes and in the induction of pancreatitis.
In this study, fat cells were detected in the exocrine pancreas of the aflatoxin-received group. A similar result was frequently observed in the pancreas during aging .
In this study, islets of Langerhans of the aflatoxin-received group appeared as pale oval areas. Most of the islets of Langerhans consisted of many cells separated by dilated congested blood capillaries. A few islet cells were vacuolated. Most of the β cells had rounded euchromatic nuclei, whereas some cells had small condensed heterochromatic nuclei. The cytoplasm of the β cells had a variety of secretory granules. Most of these granules had an electron-dense core and an electron-lucent halo, whereas some of them had homogenous moderate density. These granules sometimes coalesced. Beta cells had cytoplasmic areas depleted of granules. The current biochemical analysis for glucose and insulin showed a highly significant increase and decrease, respectively, in group II in comparison with group I. These results were similar to those detected during diabetes, glucose toxicity, and in oxidative stress [43,44]. They stated that β cells are particularly vulnerable to oxidative stress because of their low levels of antioxidant enzyme expression. This could be involved in the progression of pancreatic B-cell dysfunction, in pathological changes in pancreatic islet β cells, and in glucose toxicity [43,44]. The pancreas could not secrete insulin if the target cells lost their responsiveness to insulin; therefore, the blood glucose level increased markedly .
From the results of this study, we have concluded that aflatoxin B1 has a deleterious effect on the histological structure of the exocrine and endocrine parts of the pancreas and on the biochemical parameters that reflect the function of the pancreas. Ginger minimized these damaging effects. We recommend eating nutritious diets that contain sufficient amounts of ginger as a way to counteract the deleterious effects of the environmental exposure to pancreatic toxins such as aflatoxins. In addition, we recommend further studies on the role of ginger in aflatoxicosis in various organs.
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