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• PM produced oxidative stress in gastric, liver, and kidney tissue. • PM-induced toxicity was mediated by ROS and mitochondrial dysfunction. • PM enhanced the activated caspase-3 expression. • CoQ10 alleviates PM-induced gastropathy and hepato-renal damage. • CoQ10 might be effective in COVID-19 treatment regimen. Piroxicam (PM) is an oxicam-NSAID commonly recommended for various pain and associated inflammatory disorders. However, it is reported to have a gastric and hepato-renal toxic effect. Therefore, the current research was planned to investigate the possible mechanisms behind the mitigating action of the coenzyme (CoQ10), a natural, free radical scavenger, against PM tissue injury. Rats were assigned to five equal groups; Control, CoQ10 (10 mg/kg, orally), PM (7 mg/kg, i.p.), CoQ + PM L, and CoQ + PM H group. After 28 days, PM provoked severe gastric ulceration and marked liver and kidney damage indicated by an elevated gastric ulcer index and considerable alteration in liver and kidney biochemical tests. The toxic effects might be attributed to mitochondrial dysfunction and excess generation of reactive oxygen species (ROS), as indicated by enhanced malondialdehyde (MDA) levels along with decreased reduced-glutathione (GSH) levels and catalase (CAT) activity. Apoptotic cell death also was demonstrated by increased regulation of activated caspase-3 in the stomach, liver, and kidney tissues. Interestingly, external supplementation of CoQ10 attenuated the PM-inflicted deleterious oxidative harm and apoptosis. This ameliorative action was ascribed to the free radical scavenging activity of CoQ10. [ABSTRACT FROM AUTHOR]

Flubendiamide (FBD) is a novel diamide insecticide extensively used with potential human health hazards. This research aimed to examine the effects of FBD on PrEC prostate epithelial cells, including Oxidative stress, pro-inflammatory responses, modifications in the expression of oncogenic and suppressor miRNAs and their target proteins, disruption of the cell cycle, and apoptosis. Additionally, the research investigated the potential alleviative effect of T-SeNPs, which are selenium nanoparticles biosynthesized by Trichoderma aureoviride , against the toxicity induced by FBD. Selenium nanoparticles were herein synthesized by Trichoderma aureoviride. The major capping metabolites in synthesized T-SeNPs were Isochiapin B and Quercetin 7,3′,4′-trimethyl ether. T-SeNPs showed a spherical shape and an average size between 57 and 96.6 nm. FBD exposure (12 μM) for 14 days induced oxidative stress and inflammatory responses via overexpression of NF-κB family members. It also distinctly caused upregulation of miR-221, miR-222, and E2F2, escorted by downregulation of miR-17, miR-20a, and P27kip1. FBD encouraged PrEC cells to halt at the G 1 /S checkpoint. Apoptotic cells were drastically increased in FBD-treated sets. Treatment of T-SeNPs simultaneously with FBD revealed its antioxidant, anti-inflammatory, and antitumor activities in counteracting FBD-induced toxicity. Our findings shed light on the potential FBD toxicity that may account for the neoplastic transformation of epithelial cells in the prostate and the mitigating activity of eco-friendly synthesized T-SeNPs. [Display omitted] • FBD promoted oxidative stress and pro-inflammatory response. • FBD caused upregulation of miR-221/222 and downregulation of miR-17/20a. • FBD altered the protein level of E2F2 and P27kip1. • FBD caused cell cycle arrest at the G 1 /S checkpoint and apoptosis. • T-SeNPs rescued the insecticide's adverse effects. [ABSTRACT FROM AUTHOR]

Urine-derived stem cells (USCs) have gained the attention of researchers in the biomedical field in the past few years. Regarding the several varieties of cells that have been used for this purpose, USCs have demonstrated mesenchymal stem cell-like properties, such as differentiation and immunomodulation. Furthermore, they could be differentiated into several lineages. This is very interesting for regenerative techniques based on cell therapy. This review will embark on describing their separation, and profiling. We will specifically describe the USCs characteristics, in addition to their differentiation potential. Then, we will introduce and explore the primary uses of USCs. These involve thier utilization as a platform to produce stem cells, however, we shall concentrate on the utilization of USCs for therapeutic, and regenerative orofacial applications, providing an in-depth evaluation of this purpose. The final portion will address the limitations and challenges of their implementation in regenerative dentistry. [Display omitted] • Challenges of utilizing urine-derived stem cells for tissue engineering and regenerative medicine. • Importance of standardizing collection procedures, establishing qualifying criteria for donors, and detecting pollutants in urine. • Potential of urine-based stem cells in replacing autografts and allografts for bone defect treatments. • Differentiation potential of urine-derived stem cells and their application in orofacial tissue reconstruction. • Future directions of using urine-based stem cells in regenerative dentistry and maxillofacial surgery. [ABSTRACT FROM AUTHOR]

Aflatoxin B1 (AF) is an unavoidable environmental pollutant that contaminates food, feed, and grains, which seriously threatens human and animal health. Arabic gum (AG) has recently evoked much attention owing to its promising therapeutic potential. Thus, the current study was conducted to look into the possible mechanisms beyond the ameliorative activity of AG against AF-inflicted hepatic injury. Male Wistar rats were assigned into four groups: Control, AG (7.5 g/kg b.w/day, orally), AF (200 µg/kg b.w), and AG plus AF group. AF induced marked liver damage expounded by considerable changes in biochemical profile and histological architecture. The oxidative stress stimulated by AF boosted the production of plasma malondialdehyde (MDA) level along with decreases in the total antioxidant capacity (TAC) level and glutathione peroxidase (GPx) activity. Additionally, AF exposure was associated with down-regulation of the nuclear factor erythroid2–related factor2 (Nrf2) and superoxide dismutase1 (SOD1) protein expression in liver tissue. Apoptotic cascade has also been evoked following AF-exposure, as depicted in overexpression of cytochrome c (Cyto c), cleaved Caspase3 (Cl. Casp3), along with enhanced up-regulation of inflammatory mediators such as tumor necrosis factor-α (TNF-α), interleukin (IL)-6, inducible nitric oxide synthase (iNOS), and nuclear factor kappa-B transcription factor/p65 (NF-κB/p65) mRNA expression levels. Interestingly, the antioxidant and anti-inflammatory contents of AG may reverse the induced oxidative damage, inflammation, and apoptosis in AF-exposed animals. [ABSTRACT FROM AUTHOR]

Chronological age estimation is a challenging marker in the field of forensic medicine. The current study aimed to investigate the accuracy of signal joint T-cell receptor rearrangement excision circles (sjTRECs) quantification and telomere length measurement as methods for estimating chronological age. Telomere length was estimated in the DNA derived from the buccal cells through estimating the telomeric restriction fragment (TRF) length using TeloTTAGGG Telomere Length Assay while the sjTRECs quantification was carried out on DNA isolated from the blood samples using qPCR. The TRF length was shortened with increased age (r = −0.722, p < 0.001). The sjTRECs were also decreased with increased age (r = −0.831, p < 0.001). Stronger coefficient and lower standard error of the estimate was obtained when multiple regression analysis for age prediction based on the values of both methods was applied (r = −0.876, p < 0.001). [ABSTRACT FROM AUTHOR]

Graphical abstract Highlights • Piroxicam-induced gastric ulceration is mediated by lipid peroxidation. • Piroxicam-induced hepatorenal toxicity is mediated by lipid peroxidation. • Rosuvastatin alleviates piroxicam-inflicted gastropathy. • Rosuvastatin alleviates piroxicam-inflicted hepatorenal toxicity. • Rosuvastatin may have therapeutic potential against inflammatory diseases. Abstract Piroxicam (Px) is a non-steroidal anti-inflammatory drug that is widely prescribed in various inflammatory disorders. However, Px is known to induce gastric ulceration and hepato-renal toxicity. Rosuvastatin (ROSV), a member of the statin family, has anti-inflammatory and antioxidant actions independent of its anti-hyperlipidemic action. Therefore, we investigated the protective effects of ROSV against Px-induced gastric, liver, and kidney injury. Five groups of seven rats each were used; control group, ROSV group (20 mg/kg, given orally), Px group (7 mg/kg, given intraperitoneally), Px+ROSV L (7 and 10 mg/kg, respectively), and Px+ROSV H (7 and 20 mg/kg, respectively) group. The results revealed that Px induced severe gastric mucosal damage expressed by high ulcer index along with significant increases in liver and kidney function parameters including AST, ALT, creatinine, and urea. Disrupted lipid metabolism also was observed in Px-treated animals. Moreover, marked an increase in malondialdehyde (MDA) and decreases in glutathione (GSH) and catalase (CAT) levels along with enhanced activated caspase-3 expression in the gastric, hepatic, and renal tissues following Px-insult suggested a possible involvement of lipid peroxidation in Px-induced gastropathy and hepatorenal toxicity. However, in a dose-dependent manner, ROSV was able to mitigate Px-induced lipid peroxidation and apoptosis in gastric, liver, and kidney tissues. [ABSTRACT FROM AUTHOR]

Melamine (ML), a chemical substance of high nitrogen content, is used as a food adulterant. Former evidences implied that ML could induce a variety of toxic effects including neurotoxicity and cognitive impairment. Therefore, the aim of this study was to delineate the protective effect of the nootkatone (NK) against ML-induced neural adverse effects. Rats were orally pretreated with NK (5 and 10 mg/kg) prior to the oral administration of ML (700 mg/kg) for a period of 28 days. Our findings unveiled remarkable alleviating effect of NK on MK-induced neurobehavioral disturbance in open field test. Furthermore, NK lessened ML-caused increases in the acetylcholine esterase level in the brain tissue of exposed rats. NK also decreased the neural oxidative stress as represented by elevated levels of SOD, CAT, and GSH along with decreased MDA and NO levels. Upregulated mRNA expression levels of neural NRF-2 and HO-1 were noticed after NK administration. Remarkable anti-inflammatory impact was prominent by decreased neural IL-1β, and TNF-α along with downregulated NF-κB and TLR-4 gene expression levels in NK-treated rats. Noteworthily, pre-treatment with NK decreased the immune reaction of RAGE and HMGB-1 induced by oral ML exposure. Brain histological examination validated the obtained biochemical and molecular results. To sum up, these outcomes reveal that NK successfully alleviated the neural damage induced by ML via blocking of oxidative stress, and inflammatory signaling pathways. Consequently, our study may suggest NK as a new effective therapeutic supplement for treatment of ML-mediated neurotoxicity in rats via inhibition of HMGB-1-RAGE/TLR-4/NF-κB. • ML evoked a neuronal damage via induction of oxidative stress and inflammation. • HMGB1-RAGE/TLR-4/NF-κB signaling is involved in ML-induced neurotoxicity. • NK alleviated the ML toxicity via its antioxidant and anti-inflammatory properties. • NK acted by inhibition of HMGB1-RAGE/TLR-4/NF-κB pathway. [ABSTRACT FROM AUTHOR]

Gentamicin (GM) is a commonly prescribed antimicrobial drug used for treatment of infections but associated hepatic and renal complications restrict its efficacy. Overproduction of free radicals and inflammation are involved in GM-induced hepato-renal damage. Date palm is renowned to have antioxidant and anti-inflammatory bioactive composites. In this context, the current research was purposed to assess the ameliorative influence of date palm extract (DE) supplementation against GM-induced hepato-renal injury. Gas chromatography-mass spectrometry (GC–MS) was used to detect the bioactive constitutes in DE. The protective action of high and low doses of DE was assessed alongside the GM remediation (80 mg/kg) in rats. GM evoked significant alterations in liver and kidney function biomarkers (aminotransferases, albumin, creatinine, and blood urea). Furthermore, notable elevations in malondialdehyde (MDA) level and increment expression of inducible nitric oxide synthase (iNOS) along with reduction in catalase (CAT) activity were observed in both organs after GM treatment. Oxidative stress was the main modulatory mechanism in GM-induced hepato-renal toxicity. However, DE could mitigate the GM-inflicted liver and kidney damage, in a dose-response pattern, due to its high content of phenolics and flavonoids. [Display omitted] • Gentamicin -induced hepatorenal toxicity is mediated by lipid peroxidation. • Date palm extract alleviates gentamicin-inflicted hepatorenal toxicity in a dose-dependent pattern. • Antioxidant mechanisms are involved in such alleviation. • Date palm extract have anti-inflammatory and anti-apoptotic effect. • Date supplementation has therapeutic potential in patients receiving GM regimen. [ABSTRACT FROM AUTHOR]

CPF (chlorpyrifos) is an organophosphate pesticide used in agricultural and veterinary applications. Our experiment aimed to explore the effects of thymoquinone (TQ) and/or lycopene (LP) against CPF-induced neurotoxicity. Wistar rats were categorized into seven groups: first group served as a control (corn oil only); second group, TQ (10 mg/kg); third group, LP (10 mg/kg); fourth group, CPF (10 mg/kg) and deemed as CPF toxic control; fifth group, TQ + CPF; sixth group, (LP + CPF); and seventh group, (TQ + LP + CPF). CPF intoxication inhibited acetylcholinesterase (AchE), decreased glutathione (GSH) content, and increased levels of malondialdehyde (MDA), an oxidative stress biomarker. Furthermore, CPF impaired the activity of antioxidant enzymes including superoxide dismutase (SOD) and catalase (CAT) along with enhancement of the level of inflammatory mediators such as tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β. CPF evoked apoptosis in brain tissue. TQ or LP treatment of CPF-intoxicated rats greatly improved AchE activity, oxidative state, inflammatory responses, and cell death. Co-administration of TQ and LP showed better restoration than their sole treatment. In conclusion, TQ or LP supplementation may alleviate CPF-induced neuronal injury, most likely due to TQ or LPs' antioxidant, anti-inflammatory, and anti-apoptotic effects. [ABSTRACT FROM AUTHOR]

Aflatoxins are a common food contaminant of global concern. Aflatoxin B 1 (AFB 1) intoxication is associated with serious health hazards. Recently, fucoidan (FUC) has gained much attention from pharmaceutical industry due to its promising therapeutic effects. The impacts of FUC on AFB 1 -induced liver and kidney injures have not been sufficiently addressed. This research was conducted to evaluate the ameliorative effect of FUC in AFB1-induced hepatorenal toxicity model in rats over 14 days. Five groups were assigned; control, FUC (200 mg/kg/day, orally), AFB 1 (50 μg/kg, i.p.), and AFB 1 plus a low or high dose of FUC. AFB 1 induced marked hepatorenal injury elucidated by substantial alterations in biochemical tests and histological pictures. The oxidative distress instigated by AFB 1 enhanced production of malondialdehyde (MDA) and nitric oxide (NO) along with reduction in the reduced-glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) activities. DNA damage in the liver and kidney tissues has been demonstrated by overexpression of proliferating cell nuclear antigen (PCNA). Unambiguously, FUC consumption alleviates the AFB 1 -induced mitochondrial dysfunction, oxidative harm, and apoptosis. These ameliorated effects are proposed to be attributed to fucoidan's antioxidant and anti-apoptotic activities. Our results recommend FUC supplementation to food because it exerts both preventive and therapeutic effects against AFB 1 -induced toxicity. Unlabelled Image • Aflatoxin B 1 provoked hepatorenal injury in rat. • Aflatoxin B 1 disrupted the cellular oxidant/antioxidant balance. • Aflatoxin B 1 enhanced the expression of DNA damage and repair marker. • Fucoidan attenuated the aflatoxin B 1 toxicity via its antioxidant capability. [ABSTRACT FROM AUTHOR]