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Background: A plasticizer product, di-(2-ethylhexyl) phthalate (DEHP), is widely used in many consumer products, such as food packages, personal care products, children` toys, and medical devices. Phthalates are known to be released into the biological fluids and redistributed into various tissues linked with multiple health problems.Aim: We aimed to study the possible toxic effect of phthalate exposure on the lung tissues.Methods: Thirty male Wister rats were randomly divided into three groups equally, received the following for two weeks once daily via gastric intubation: control group; received normal saline. The DEHP treated group received 2,85mg/kg per BW of DEHP dissolved in normal saline. The DEHP recovery group, received the same as the treated group, followed by two weeks without any treatment. For light microscopic study; the lung tissues were dissected, cut into small pieces, processed, embedded in paraffin wax, sectioned and stained with Hematoxylin and Eosin as well as Masson trichrome stains. For electron microscopic study; the lung tissues were fixed in glutaraldehyde, processed, embedded in epoxy, cut into ultrathin sections, and stained with uranyl acetate and lead citrate.Results: Compared to the control group, the alveolar tissues in the treated group showed a significant increase in collagen deposition and inflammatory cellular infiltration. The number of type-II pneumocytes and alveolar macrophages/field were also significantly increased. However, these pathological changes improved slightly after stopping exposure to DEHP.Conclusion: DEHP has a toxic effect on the lung tissues, which after its withdrawal did not improve completely.

BackgroundAcute renal failure (ARF) is a common clinical problem with grave prognosis and limited therapeutic modalities. Current therapeutic options for ARF are limited to supportive procedures and preventive care, none of which have been definitively shown to alter mortality.ObjectiveThe purpose o

Introduction: The non-steroidal anti-inflammatory drug (NSAID) Piroxicam is widely used especially in treatment of osteoarthritis and rheumatoid arthritis. However, it has many side effects; the most common of them is gastrointesti nal intolerance and ulceration. The Nigella Sativa Oil (NSO) was reported to have anti-inflammatory and antioxidant properties. Aim of the Work: To investigate the histopathological effects of piroxicam on the gastric mucosa of adult male albino rats and the possible protective role of Nigella Sativa Oil (NSO). Materials and Methods: Fourty adult male albino rats were randomized into 4 groups (NN10). They received 2 ml of the following oral treatments through an orogastric tube: Group I (Control) received a single dose of saline, Group II (NSO) received a single dose of NSO; 10 ml/kg BW, Group III (Piroxicam) received piroxicam 20 mg/kg BW and Group IV (NSO/ piroxicam) received NSO one hour before administration of piroxicam. The gastric mucosa from the body of the stomach was processed for histological stains (H&E and PAS) and for examination with scanning electron microscope (SEM). Results: Piroxicam produced erosions, congestion, extravasated RBCs and inflammatory cell infiltration. It also led to increase in the gastric mucus. The SEM results revealed marked damage of the gastric mucosal surface and complete loss of the normal architecture. In NSO prior to piroxicam group, the structure of the mucosa was nearly similar to control by both light and SEM however, there was marked increase in mucus secretion. Conclusion: NSO can partly protect the gastric mucosa against piroxicam induced damage.

Background: DEHP is a commonly used phthalate plasticizer in polyvinylchloride (PVC) formulations used by many medical devices. It is known to be released with time into the biological fluids or redistributed into various tissues increasing the risk of certain health hazards that include developmental anomalies, reproductive and respiratory health effects. Objective: To investigate the histopathological effects of DEHP on the lung alveolar tissues and the possibility of recovery after stoppage of DEHP administration in adult albino rats. Methods: Thirty adult male albino rats were divided equally into three groups, received the following via orogastric intubation once daily for 2 weeks: Group I (control group): received normal saline. Group II (DEHP treated group): received DEHP dissolved in normal saline. Group III (DEHP recovery group): received DEHP as group II and then left untreated for another 2 weeks. The right lung from each animal was dissected, cut into small pieces. Some specimens were processed for paraffin sections to be stained with Haematoxylin & Eosin and Masson’s trichrome, others were processed for semi-thin sections, and ultrathin sections to be examined with Transmission Electron Microscope. Results: The alveolar tissue in DEHP treated group showed marked increase in the thickness of the interalveolar septa with collagen deposition and inflammatory cellular infiltration associated with many collapsed alveoli. Most of type II pneumocytes showing necrotic changes in the form of vacuolated or deeply acidophilic cytoplasm with karyorrhetic or pyknotic nuclei. Additionally, there was interstitial hemorrhage. We found a statistically significant increase in the thickness of the interalveolar septa, number of type II pneumocyte, number of alveolar macrophages/field and the area percentage of collagen fibers when compared to control group. Ultrastructurally, type II pneumocytes showed degenerative changes in the form of cytoplasmic vacuolation and destruction of lamellar bodies and mitochondria. However, alveolar tissue changes showed mild improvement after drug stoppage. Conclusion: DEHP has toxic effect on the alveolar tissues which was not totally improved after its withdrawal.