Background: Much consideration has been paid to the toxicological assessment of nanoparticles prior to clinical and biological applications. While in vitro studies have been expanding continually, in vivo investigations of nanoparticles have not developed a cohesive structure. This study aimed to assess the acute toxicity of different concentrations of chitosan-coated silver nanoparticles (Ch-AgNPs) in main organs, including liver, kidneys, and spleen. Materials and methods: Twenty-eight male albino rats were used and divided into 4 groups (n=7). Group 1 was kept as a negative control group. Groups 2, 3, and 4 were treated intraperitoneally with Ch-AgNPs each day for 14 days at doses of 50, 25, and 10 mg/kg body weight (bwt) respectively. Histopathological, morphometric and immunohistochemical studies were performed as well as oxidative stress evaluations, and specific functional examinations for each organ were elucidated. Results: It was revealed that Ch-AgNPs induced dose-dependent toxicity, and the repeated dosing of rats with 50 mg/kg Ch-AgNPs induced severe toxicities. Histopathological examination showed congestion, hemorrhage, cellular degeneration, apoptosis and necrosis in hepatic and renal tissue as well as lymphocytic depletion with increasing tangible macrophages in the spleen. The highest levels of malondialdehyde, alanine aminotransferase, aspartate aminotransferase (MDA, ALT, AST) and the lowest levels of reduced glutathione, immunoglobulin G, M and total protein (GSH, IgG, IgM, TP) were observed in this group. On the other hand, repeated dosing with 25 mg/kg induced mild to moderate disturbance in the previous parameters, while there was no significant difference in results of pathological examination and biochemical tests between the control group and those treated with 10 mg/kg bwt Ch-AgNPs. Conclusion: Chitosan-coated silver nanoparticles induce dose-dependent adverse effects on rats.

In forensic medicine, it is vital to verify with the best attainable accuracy once injuries occurred during vital or post‐mortem conditions. An immunohistochemical study was carried out to examine the time‐dependent expression of macrophage‐specific gene CD68 (cluster of differentiation 68), alpha‐smooth muscle actin (α‐SMA), and vascular endothelial growth factor (VEGF) in different skin wound timings (0, 1, 3, 5, 7, and 14 days) in rats. Histopathological studies were performed to assess the wound age and vitality. Eighteen male albino Wister rats (weighing 170‐200 g) were used for wound induction. Rats (n = 3) were euthanised at 0, 1, 3, 5, 7, and 14 days from the starting point of wound induction. Histopathological examination showed that the epidermal re‐epithelialisation was completed 14 days after skin incision. The inflammatory phase was recorded during the first 3 days of healing and reached the maximum levels at 5 days, then declined after 7 days, and completely removed at 14 days. The beginning of the proliferative phase was dated to day 3 and the peak at days 5 and 7. The initiation of the granulation tissue formation and remodelling phase of the healing process was observed 5 days after wounding. By immunohistochemical staining, negative VEGF gene expressions at early stages (0‐3 days) were observed, as well as neither CD68+ macrophages nor α‐SMA+ myofibroblast cells were detected. By increasing the wound ages (5‐7 days), granulation tissue and angiogenesis were observed, with the migration of macrophages and fibroblast, which expressed VEGF, CD68, and α‐SMA positive reaction. Time‐dependent expression of the above markers suggested that they would be useful indicators for the determination of wound age. Both VEGF and transforming growth factor‐beta 1 (TGFb1) mRNA levels were determined in different skin wound ages. The transcription of TGFb1 and VEGF increased shortly after wounding, until post‐wounding day 7. It then declined constantly, reaching minimal values on day 14.

Background: Pomegranate (Punica granatum L) has been used since ancient times in the traditional medicine of several cultures, particularly in the Middle East. It is an essential commercial crop full of bioactive compounds with several medical applications. Pomegranate is very popular for its biological effects exerted by phenolic compounds via free radical scavenging abilities. It has revealed high antioxidant and anti-inflammatory activities and is beneficial for the amelioration of liver and kidney diseases. Purpose: To elucidate the potential efficacy of pomegranate juice (PJ) against copper oxide nanoparticles (CuO-NPs)-induced apoptosis, inflammation, and oxidative stress damage. Study design: 37 nm sized CuO-NPs were prepared by precipitation method and characterized by using X-ray diffractometer (XRD), Zetasizer nano-and high-resolution transmission electron microscope (HR-TEM). 30 Wistar rats were partitioned into 6 equal groups as follows: Group 1 (negative control), groups 2 & 3 (PJ control groups), group 4 (CuO-NPs group), groups 5 & 6 (CuO-NPs + PJ groups). Methods: Hepato-renal protective effect of PJ was evaluated by measuring levels of serum marker enzymes (ALT, AST,blood urea nitrogen and creatinine). Cu NPs bioaccumulation in liver and kidneys was determined by using atomic absorption spectrophotometer. The oxidative stress markers, Rt-PCR analysis, histopathological and immunohistochemical studies were carried out in the liver and kidneys to support the above parameters. Results: Rats injected with CuO-NPs showed higher levels of the above serum marker enzymes, alteration of oxidant–antioxidant balance together with severe pathological alterations in liver and kidney tissues and overexpression of both caspase-3 and nuclear factor kappa B protein (NF-ĸB) associated with upregulation of Bax gene and downregulation of Bcl2 gene in these organs. PJ ameliorated all of the above toxicological parameters. Conclusion: PJ was proved to be a potential hepato-renal protective agent against liver and kidney damage induced by CuO-NPs via its antioxidant, anti-inflammatory, and anti-apoptotic effects.

Pesticides are viewed as a major wellspring of ecological contamination and causing serious risky consequences for people and animals. Imidacloprid (IM) and hexaflumuron (HFM) are extensively utilized insect poisons for crop assurance on the planet. A few investigations examined IM harmfulness in rodents, but its exact mechanism hasn’t been mentioned previously as well as the toxicity of HFM doesn’t elucidate yet. For this reason, the present study was designed to explore the mechanism of each IM and HFM–evoked rat liver and kidney toxicity and to understand its molecular mechanism. 21 male Wistar albino rats were divided into 3 groups, as follows: group (1), normal saline; group (2), IM; and group (3), HFM. Both insecticides were orally administered every day for 28 days at a dose equal to 1/10 LD50 from the active ingredient. After 28 days postdosing, rats were anesthetized to collect blood samples then euthanized to collect liver and kidney tissue specimens. The results showed marked changes in walking, body tension, alertness, and head movement with a significant reduction in rats’ body weight in both IM and HFM receiving groups. Significant increases in MDA levels and decrease of GHS levels were recorded in liver and kidney homogenates of either IM or HFM groups. Liver and kidney tissues obtained from both pesticide receiving groups showed extensive histopathological alterations with a significant increase in the serum levels of ALT, AST, urea, and creatinine and a decrease in total proteins, albumin, and globulin levels. In addition, there was upregulation of the transcript levels of casp-3, JNK, and HO-1 genes with strong immunopositivity of casp-3, TNF-ὰ, and NF-_KB protein expressions in the liver and kidneys of rats receiving either IM or HFM compared with the control group. In all studied parameters, HFM caused hepatorenal toxicity more than those induced by IM. We can conclude that each IM and HFM provoked liver and kidneys damage through overproduction of ROS, activation of NF-_KB signaling pathways and mitochondrial/JNK-dependent apoptosis pathway.

This study aimed to evaluate what dosage of gold nanoparticles (GNPs) would improve growth performance, antioxidant levels and immune defense in broiler chickens. The experiment was carried out on 90 one-day-old mixbred Cobb chicks. The birds were allocated into three groups with three replicates. Group (1) kept as a negative control. Groups (2) and (3) received 5, 15 ppm GNPs via drinking water weekly for 35 days of chicks' life. Blood samples were collected at 8, 15, 22 and 36 days for oxidative stress evaluations and immunological studies. The birds were slaughtered at the ages of 36 days and thymus, spleen, busa of Fabricius and liver were collected for histopathological description, RT-PCR analysis and DNA fragmentation assay. Our results confirmed that adding of 15ppm GNPs in drinking water were induced remarkable blood oxidative stress damage, histopathological alterations, up-regulation of IL-6, Nrf2 gene expression, and DNA fragmentation in the examined immune organs of the broiler chickens as well as a significant reduction in the antibody titer against Newcastle (ND) and avian influenza (AI) viruses were noticed. On the other hand, the group received 5ppm GNPs noticed better growth performance with the enhancement of the final food conversion ratio (FCR) without any significant difference in the previous toxicological and immunological parameters compared to the control groups. We suggest that feeding of 5ppm GNPs could improve the antioxidant capacity, immunity and performance in poultry but further food quality assurance tests are required in the future to confirm its safety for people.