El-Shater, S. N., K. Abo-EL-Sooud, A. tolba, M. Gamal, M. A. Awad, M. Ibrahim, M. Tayeh, and G. A. Swielim, "Effect of in-ovo inoculation of betaine on hatchability, serum antioxidant levels, muscle gene expression and intestinal development of broiler chicks.", Journal of animal physiology and animal nutrition, 2024. Abstract

This study investigated the effects of in-ovo inoculation of betaine on hatchability, hatching weight, and intestinal development, as well as serum and expression levels of some antioxidants in the posthatched chicks. A total of 350 fertile eggs of Hubbard efficiency plus breeder's flock were incubated at normal incubation temperature (37.5°C) and randomly assembled into 3 groups with 4 replicates, and 25 eggs per each. The experimental groups were allocated as noninjected control group (CN), diluent-injected group (CP, 0.1 mL saline), and betaine-injected group (B, 2.5 mg in 0.1 mL saline). The injections were performed in the air cells of the eggs on the 12th day of the embryonic phase. Hatchability percentage, hatching weight, serum-reduced glutathione (GSH), and superoxide dismutase (SOD) were estimated in 7-day-old chicks. Moreover, expression levels of the nuclear factor erythroid 2-related factor 2 (Nrf2) and SOD were determined in the breast skeletal muscles of chicks. Jejunum histo-morphometric analysis was assessed with computerised morphometric measurements. The results revealed that the hatchability percentage was not influenced by in-ovo injection of betaine or vehicle while betaine significantly increased the hatchling's weight of chicks. Moreover, there were a significant increase in SOD and Nrf2 mRNA expression levels. In-ovo injection of betaine significantly induced positive effects on intestinal morphometry by ameliorating the jejunal villus length, the ratio of villus height to villus width, and absorptive surface area.

Behairy, A., M. M. M. Hashem, K. Abo-EL-Sooud, A. M. Soliman, S. M. Mouneir, A. E. El-Metwally, S. H. Ismail, B. A. Hassan, and Y. M. Abd-Elhakim, "Influence of titanium dioxide nanoparticles and/or cadmium chloride oral exposure on testicular morphology, oxidative stress, and apoptosis in rats: Ameliorative role of co-enzyme Q10.", Heliyon, vol. 10, issue 1, pp. e24049, 2024. Abstractheliyon.pdf

BACKGROUND AND OBJECTIVES: Little is known about the implications of titanium dioxide nanoparticles (TiONPs) and cadmium chloride (Cd) co-exposure on the male reproductive system in mammals. As a result, this study researched the effects of oral TiONPs and/or Cd exposure on male reproduction and testicular functions. Additionally, a mitigation trial with co-enzyme Q10 (CoQ10) has also been conducted.

METHODS: In a 60-day experiment, seven experimental groups, each containing 10 male Sprague Dawley rats, were orally given distilled water (control), corn oil (vehicle control), CoQ10 (10 mg/kg b.wt), TiONPs (50 mg/kg b.wt), Cd (5 mg/kg b.wt), TiONPs + Cd, and TiONPs + Cd + CoQ10. Then, sperm quality, male sex hormones, oxidative stress indications, Ti and Cd testicular residues, testes and accessory gland architecture, and apoptotic and inflammatory markers in rat testes were assessed.

RESULTS: TiONPs and/or Cd exposure negatively impacted body weight, weight gain, testicular weights, semen quality, serum reproductive hormones, oxidative stress parameters, and Caspase-3 and tumor necrosis factor (TNF-α) immunoreactions. Histopathological changes were recorded in testicular, seminal vesicle, and prostatic tissues. Yet, co-administration of CoQ10 with TiONPs and Cd substantially mitigated these adverse consequences. The most notable aspect is that it effectively lowered testicular tissue Ti and Cd levels. It also improved oxidant status, hormonal profile, and sperm picture. CoQ10 minimized the testicular damage implied by histological examination. Furthermore, CoQ10 significantly diminished TiONPs and Cd-induced Caspase-3 and TNF-α immunoexpression in testicular tissue.

CONCLUSION: As a result, CoQ10 could be utilized as a safe remedy to protect male reproductive physiology from TiONPs and Cd damage.

Bahr, M. M., M. Samer, K. Abo-EL-Sooud, S. M. Kamel, M. A. Fouly, A. N. Abdallah, A. A. Shamaa, and O. S. el-Tookhy, "Effect of Topical application of Lyophilized Xenogenous Mesenchymal Stem Cell-Derived Extracellular Vesicles on Central and Peripheral Corneal Ulcers Healing in Rabbits", Adv. Anim. Vet. Sci., vol. 11, issue 1, pp. 132-140, 2023.
A.Hassan;, M. H. E. - K.; E., O. El-Tookhy;, D. S.A.;, G. G. S., and Ashraf A. Shamaa, "Use of heterogeneous differentiated mesenchymal stem cells as a cirrhotic liver cell therapy of: a canine model Experimental study.", Proceeding of 4th international conference on tissue science and regenerative medicine, July 27-29 Rome, 2015. Abstract
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Abd-Elhakim, Y. M., M. M. M. Hashem, K. Abo-EL-Sooud, M. R. Mousa, A. M. Soliman, S. M. Mouneir, S. H. Ismail, B. A. Hassan, and H. H. M. El-Nour, "Interactive effects of cadmium and titanium dioxide nanoparticles on hepatic tissue in rats: Ameliorative role of coenzyme 10 via modulation of the NF-κB and TNFα pathway.", Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, vol. 182, pp. 114191, 2023. Abstractfood_and_chemical_toxicology.pdf

This study investigated the effect of oral dosing of titanium dioxide nanoparticles (TNPs) and cadmium (Cd) on rat liver and the potential protective role of coenzyme Q10 (CQ10) against TNPs and Cd-induced hepatic injury. Seventy male Sprague Dawley rats were divided into seven groups and orally given distilled water, corn oil, CQ10 (10 mg/kg b.wt), TNPs (50 mg/kg b.wt), Cd (5 mg/kg b.wt), TNPs + Cd, or TNPs + Cd+CQ10 by gastric gavage for 60 successive days. The results showed that individual or mutual exposure to TNPs and Cd significantly increased the serum levels of various hepatic enzymes and lipids, depleted the hepatic content of antioxidant enzymes, and increased malondialdehyde. Moreover, the hepatic titanium and Cd content were increased considerably in TNPs and/or Cd-exposed rats. Furthermore, marked histopathological perturbations with increased immunoexpression of tumor necrosis factor-alpha and nuclear factor kappa B were evident in TNPs and/or Cd-exposed rats. However, CQ10 significantly counteracted the damaging effect of combined exposure of TNPs and Cd on the liver. The study concluded that TNPs and Cd exposure harm hepatic function and its architecture, particularly at their mutual exposure, but CQ10 could be a candidate protective agent against TNPs and Cd hepatotoxic impacts.

Abo-EL-Sooud, K., Y. M. Abd-Elhakim, M. M. M. Hashem, A. E. El-Metwally, B. A. Hassan, and H. H. M. El-Nour, "Restorative effects of gallic acid against sub-chronic hepatic toxicity of co-exposure to zinc oxide nanoparticles and arsenic trioxide in male rats.", Heliyon, vol. 9, issue 6, pp. e17326, 2023. Abstractheliyon.pdf

BACKGROUND AND OBJECTIVES: This study aimed to assess the effect of zinc oxide nanoparticles (ZNPs) and/or arsenic trioxide (ATO) exposure on the liver of adult male Sprague Dawley rats. Moreover, the probable ameliorative impact of gallic acid (GA) against ZNPs and ATO-induced hepatotoxicity and the possible underlying mechanisms were evaluated.

METHODS: Sixty male Sprague Dawley rats were distributed into six groups. The 1 and 2 groups were orally given distilled water (1 ml/kg) and 20 mg GA/kg b. wt, respectively. The 3 and 4 groups were orally given 100 mg ZNPs/kg b. wt and 8 mg ATO/kg b. wt, respectively. The 5 group was co-administered ZNPs and ATO at the doses mentioned above. The last one was co-administered ZNPs, ATO, and GA at the earlier described doses. All tested compounds were orally given once a day for 60 successive days. Then, serum levels of alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), total, direct, indirect bilirubin, triglycerides, total cholesterol, HDL, VLDL, and LDL were estimated. The hepatic content of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPx) was evaluated. Moreover, Bcl-2 and Bax's reactive proteins were immunohistochemically detected, and Zn and As residual patterns in hepatic tissues were assessed.

RESULTS: ZNPs, ATO, and ZNPs+ATO-exposed rats showed significantly ( < 0.001) elevated serum AST (219%, 233%, and 333%), ALT (300%, 400%, and 475%), ALP (169%, 205%, and 294%), and total bilirubin (42%, 68%, and 109%) compared to the control ones. On the other hand, a significantly ( < 0.001) declined SOD (58%, 49%, and 43%) and GPx (70%, 63%, and 56%) but increased MDA (133%, 150%, and 224%) was recorded in the hepatic tissues of ZNPs, ATO, and ZNPs+ATO exposed rats, respectively, relative to the control rats. Moreover, the hepatic tissues of the ZNPs, ATO, and ZNPs+ATO exposed rats showed a significant ( < 0.001) decrease in Bcl-2 (28%, 33%, and 23%) but elevation in Bax (217%, 267%, and 236%) immunoreactivities compared to the control rats. These findings were consistent with the microscopic alterations in the hepatic architecture and accumulation of Zn and As. Furthermore, a notable hyperlipidemic condition was recorded following ZNPs and/or ATO exposure. On the contrary, GA notably reduced hepatic enzymes compared to ZNPs+ATO-exposed rats. Additionally, GA markedly improved ZNPs+ATO-afforded liver tissue damage and apoptotic events.

CONCLUSION: Overall, GA oral dosing significantly mitigated the negative effects of ZNPs and ATO on the liver by improving the antioxidant defense system and controlling apoptotic changes.

Abd-Elhakim, Y. M., A. Behairy, M. M. M. Hashem, K. Abo-EL-Sooud, A. E. El-Metwally, B. A. Hassan, and H. A. Ali, "Toll-like receptors and nuclear factor kappa B signaling pathway involvement in hepatorenal oxidative damage induced by some food preservatives in rats.", Scientific reports, vol. 13, issue 1, pp. 5938, 2023. Abstracttoll_like__receptors.pdf

Chemical food preservatives are extensively found in various processed food products in the human environment. Hence, this study aimed to investigate the effect of long-term exposure to five food preservatives (potassium sorbate (PS), butylated hydroxyanisole (BHA), sodium benzoate (SB), calcium propionate (CP), and boric acid (BA)) on the liver and kidney in rats and the probable underlying mechanisms. For 90 days, sixty male albino rats were orally given either water (control), 0.09 mg/kg b.wt BHA, 4.5 mg/kg b.wt PS, 0.9 mg/kg b.wt SB, 0.16 mg/kg b.wt BA, or 0.18 mg/kg b.wt CP. Liver and kidney function tests were assessed. Hepatic and renal oxidative stress biomarkers were estimated. Histologic examination analysis of liver and kidney tissues was achieved. Toll-like receptors 2 and 4 (TLR-2 and TLR-4), tumor necrosis factor-alpha (TNF-α), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) mRNA expression levels were measured. The results revealed that long-term oral dosing of the five food preservatives resulted in significant increases in alkaline phosphatase, alanine transaminase, aspartate transaminase, urea, uric acid, and creatinine levels. There were significant reductions in hepatic and renal antioxidant enzymes, an increase in MDA concentrations, and pathological alterations in renal and hepatic tissues. The mRNA levels of TLR-4, TLR-2, NF-κB, and TNF-α were elevated in the food preservatives-exposed groups. Conclusively, the current findings revealed that long-term exposure to PS, BHA, SB, CP, and BA has a negative impact on liver and kidney function. Furthermore, these negative effects could be mediated via oxidative stress induction, inflammatory reactions, and cytokine production.

Abo-EL-Sooud, K., Y. M. Abd-Elhakim, M. M. M. Hashem, A. E. El-Metwally, B. A. Hassan, and H. H. M. El-Nour, "Ameliorative effects of quercetin against hepatic toxicity of oral sub-chronic co-exposure to aluminum oxide nanoparticles and lead-acetate in male rats.", Naunyn-Schmiedeberg's archives of pharmacology, vol. 396, issue 4, pp. 737-747, 2023. Abstractnaunyn-schmiedebergs_archives_of_pharmacology.pdf

The present study was designed to evaluate the probable ameliorative role of quercetin (QCN) against oxidative hepatotoxicity induced by aluminum oxide nanoparticles (AlONPs) with a diameter < 30 nm and lead acetate (Pb) co-exposure in adult male Sprague-Dawley rats. Rats were weighed and allocated to seven groups (n = 10 each) and were treated orally via orogastric gavage for 60 successive days: rats of the 1st group were kept as control given distilled water (1 ml/kg), rats of the 2nd group received 2 ml/kg BW/day corn oil; rats of the 3rd group were administered 20 mg/kg BW QCN/day; rats of the 4th group received 100 mg/kg BW AlONPs; rats of the 5th group received 50 mg/kg BW Pb; rats of the 6th group co-received AlONPs and Pb at the same previous doses; and rats of the 7th group were co-administered AlONPs, Pb, and QCN at the same previous doses. At the end of the experiment, serum levels of alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), total, direct, indirect bilirubin, triglycerides, total cholesterol, HDL, VLDL, and LDL were estimated. The hepatic oxidative stress biomarkers as superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GPx), were also evaluated. Finally, the histopathological and histomorphometric evaluations and the residues of Al and Pb in hepatic tissues were assessed. AlONPs and/or Pb exposure significantly elevated lipid peroxidation levels and considerably altered the hepatic biochemical parameters; nevertheless, QCN significantly reduced hepatic enzymes compared to toxicant exposed groups. Additionally, QCN significantly improved AlONPs-afforded liver tissue damage, as established in microscopic findings on the liver in the group treated with AlONPs + Pb. Conclusively, QCN could be a candidate natural agent to safeguard the liver versus the co-harmful impacts of AlONPs and Pb toxicity.

Behairy, A., M. M. Hashem, K. Abo-EL-Sooud, A. E. El-Metwally, B. A. Hassan, and Y. M. Abd-Elhakim, "Quercetin Abates Aluminum Trioxide Nanoparticles and Lead Acetate Induced Altered Sperm Quality, Testicular Oxidative Damage, and Sexual Hormones Disruption in Male Rats.", Antioxidants (Basel, Switzerland), vol. 11, issue 11, 2022. Abstractantioxidants-11-02133.pdf

This study examined the effects of exposure to lead acetate (PbAc) and/or aluminum trioxide nanoparticles (AlONPs) on testicular function. Additionally, the probable reproprotective effects of quercetin (QTN) against AlONPs and PbAc co-exposure in male Sprague Dawely rats were assessed. AlONPs (100 mg/kg b.wt.), PbAc (50 mg/kg b.wt.), and QTN (20 mg/kg b.wt.) were orally administered for 60 days. Then, spermiogram, histopathological examinations of the testis and accessory glands, and immunohistochemical detection of androgen receptors (AR) and tumor necrotic factor alpha (TNF-α) were achieved. Moreover, serum levels of male sex hormones and testicular levels of antioxidant indices were estimated. The results showed that AlONP and/or PbAc caused significant sperm abnormalities, testicular oxidative stress, and histopathological changes. Furthermore, serum testosterone, LH, and FSH levels significantly decreased, while estradiol levels significantly increased. The AlONPs and/or PbAc co-exposed group had more obvious disturbances. Furthermore, QTN co-administration significantly reversed the AlONPs and PbAc-induced testicular histopathological alterations, reduced antioxidant defenses, and altered AR and TNF-α immune expression in testicular tissues. Conclusively, AlONPs and/or PbAc evoked testicular dysfunction by inducing oxidative injury and inflammation. However, QTN oral dosing effectively mitigated the negative effects of AlONPs and PbAc by suppressing oxidative stress and inflammation and improving the antioxidant defense system.

Kumar, S., J. Saxena, V. K. Srivastava, S. Kaushik, H. Singh, K. Abo-EL-Sooud, M. M. Abdel-Daim, A. Jyoti, and R. Saluja, "The Interplay of Oxidative Stress and ROS Scavenging: Antioxidants as a Therapeutic Potential in Sepsis.", Vaccines, vol. 10, issue 10, 2022. Abstractvaccines-10-01575.pdf

Oxidative stress resulting from the disproportion of oxidants and antioxidants contributes to both physiological and pathological conditions in sepsis. To combat this, the antioxidant defense system comes into the picture, which contributes to limiting the amount of reactive oxygen species (ROS) leading to the reduction of oxidative stress. However, a strong relationship has been found between scavengers of ROS and antioxidants in preclinical in vitro and in vivo models. ROS is widely believed to cause human pathology most specifically in sepsis, where a small increase in ROS levels activates signaling pathways to initiate biological processes. An inclusive understanding of the effects of ROS scavenging in cellular antioxidant signaling is essentially lacking in sepsis. This review compiles the mechanisms of ROS scavenging as well as oxidative damage in sepsis, as well as antioxidants as a potent therapeutic. Direct interaction between ROS and cellular pathways greatly affects sepsis, but such interaction does not provide the explanation behind diverse biological outcomes. Animal models of sepsis and a number of clinical trials with septic patients exploring the efficiency of antioxidants in sepsis are reviewed. In line with this, both enzymatic and non-enzymatic antioxidants were effective, and results from recent studies are promising. The usage of these potent antioxidants in sepsis patients would greatly impact the field of medicine.