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Titanium dioxide nanoparticles (TiO 2 NPs) are extensively incorporated in numerous industrial products. Adult male Albino rats received oral TiO 2 NPs at a dose of 150 mg/kg body weight for 14 days exhibited both hepatic and renal toxicities manifested by disruption in serum hepatic and renal biomarkers, imbalance in oxidative-antioxidant system, up-regulation of mRNA expression of genes encode inflammation (IL-1β, TNF-α) and apoptosis (Caspase-3, BAX) with down-regulation of PCNA immune-staining density and histological modifications in hepatic and renal architecture. Carboxymethyl chitosan (5 mg/kg BW) significantly improved the harmful effects of nano-titanium particles highlighting its relevance in reducing TiO 2 NPs – induced hepatic and renal dysfunction.

This study aimed to assess the possible consequences of spirulina (SP) and/or L-carnitine (L-car) on the prevention of primordial follicular reserve depletion and the preservation of ovarian follicular structure and function in a rat model of premature ovarian insufficiency (POI). Forty healthy adult female Sprague-Dawley albino rats were randomly assigned into five equal-sized groups ( n  = 8): normal control, DOX group (2.5 mg/kg i.p.), SP group (500 mg/kg intragastric), L-car group (250 mg/kg i.p.), and SP + L-car group in the same previous doses. In comparison to the DOX group, administration of either SP or L-car significantly increased serum E2 and AMH levels along with a significant decrease in the FSH and LH levels ( p <  0.05). The oxidative stress was significantly reduced. Ovarian expressions of NF-κB, iNOS, FOXO1, P53, and caspase-3 decreased significantly, while SIRT1, STAR, CYP17A1, HSD17B3, Nrf2, and mtDNA increased significantly. Histology revealed histoarchitecture improvement as the mean % of atretic follicles and degenerated corpora lutea was significantly reduced ( p <  0.05). The combined treatments synergistically improved the parameters studied more than either treatment alone. The molecular docking results revealed the ability of both n-hexadecanoic acid and L-carnitine to activate SIRT1 and subsequent antioxidant, anti-inflammatory, and anti-apoptotic pathways. This ovoprotective effect is suggested to be mediated through activation of different SIRT1-mediated protective signaling pathways that remodel ovarian redox status, inflammation, and apoptosis, which may strengthen the potential role of SP and L-car as a chemotherapy adjuvant, reducing the negative health effects of early menopause after cancer therapy.

The potential reproductive toxic effects of oral TiO 2 NPs in adult male rats as well as the possible alleviation of chitosan administration was investigated. Animals were allocated to four groups; the first group received deionized water and was assigned as a control group. In the second group, rats received chitosan at a dose of 5 mg/kg BW/day. The third group was designed for administration of TiO 2 NPs at a dose of 150 mg/kg BW/day (1/80 LD 50 ). Rats in the fourth group received both TiO 2 NPs and chitosan. After 14 days, TiO 2 NPs induced testicular lipid peroxidation as well as oxidative stress. Nano-titanium significantly upregulated genes that encode apoptosis and inflammation in testicular tissue. Moreover, it induced histological alteration in the testicular structure with impairment in spermatogenesis via reduction of PCNA immune-staining. Chitosan administration significantly improved the activities of testicular GPx, SOD, and CAT enzymes. In addition, it significantly down-regulated the relative expressions of pro-apoptotic and pro-inflammatory testicular genes. Chitosan was able to improve the testicular architecture as well as spermatogenesis. The current study revealed the capability of chitosan to ameliorate nano-titanium induced testicular toxicity. Thus, attention should be given to the extensive consumption of nano-titanium particles.

Aims We investigated the effects of intraperitoneal injections of titanium dioxide nanoparticles (TiO 2 NPs, 100 mg/kg) for 5 consecutive days on the developmental competence of murine oocytes. Furthermore, study the effects of TiO 2 NPs on antioxidant and oxidative stress biomarkers, as well as their effects on expression of apoptotic and hypoxia inducing factor-1α ( HIF1A ) protein translation. Moreover, the possible ameliorating effects of intraperitoneal injections of fructose (2.75 mM/ml) was examined. Materials and methods Thirty sexually mature (8–12 weeks old; ~ 25 g body weight) female mice were used for the current study. The female mice were assigned randomly to three treatment groups: Group1 (G1) mice were injected intraperitoneal (ip) with deionized water for 5 consecutive days; Group 2 (G2) mice were injected ip with TiO 2 NPs (100 mg/kg BW) for 5 consecutive days; Group 3 (G3) mice were injected ip with TiO 2 NPs (100 mg/kg BW + fructose (2.75 mM) for 5 consecutive days. Results Nano-titanium significantly decreased expression of GSH, GPx, and NO, expression of MDA and TAC increased. The rates of MI, MII, GVBD and degenerated oocytes were significantly less for nano-titanium treated mice, but the rate of activated oocytes was significantly greater than those in control oocytes. TiO 2 NPs significantly increased expression of apoptotic genes ( BAX, Caspase 3 and P53 ) and HIF1A. Intraperitoneal injection of fructose (2.75 mM/kg) significantly alleviated the detrimental effects of TiO 2 NPs. Transmission electron microscopy indicated that fructose mitigated adverse effects of TiO2 NPs to alter the cell surface of murine oocytes. Conclusion Results of this study suggest that the i/p infusion of fructose for consecutive 5 days enhances development of murine oocytes and decreases toxic effects of TiO 2 NPs through positive effects on oxidative and antioxidant biomarkers in cumulus-oocyte complexes and effects to inhibit TiO2-induced increases in expression of apoptotic and hypoxia inducing factors.

BackgroundSpinal cord injury (SCI) is widely considered the most disastrous medical condition. With no available treatment to date, SCI continues to cause disabilities to the patients and affect their own and their caregivers' quality of life. Cerebrolysin (CBL) is a neuropeptide preparation derived from purified brain proteins with suggested neuroprotective and neurotrophic properties. CBL showed earlier the ability to target multiple pathways that helped in the improvement of the recovery following different groups of neurological diseases and injuries, including ischemic stroke, traumatic brain injuries, and even neurodegenerative diseases. In the current study, the neuroprotective effect of CBL following a SCI is called into question using a rat model of spinal cord cervical hemi-section validated earlier by our lab and others. Using 32 rats divided into four groups randomly, CBL treatment was implemented for either 7 or 21 days duration, following the cervical spinal cord hemi-section.ResultsFollowing the CBL treatment, rats with cervical cord hemi-section showed functional improvement of diaphragmatic muscle as recorded by electromyography (EMG). In addition, the histopathological assessment of the spinal cord showed improved neuronal viability and reduced astrogliosis at the site of the injury compared to the non-treated group. 21-day treatment showed significant improvement when compared to the shorter 7-day regimen.ConclusionOur data suggest that CBL is capable of protecting and regenerating anterior horn motor neurons with functional recovery of diaphragmatic muscle functions in rats, suggesting the potential use of CBL for future regenerative and neuroprotective therapy following SCI.

The experiment was designed to examine the influence of employing three doses of ZnSO 4 on the wound healing process in partially scaled common carp. A total of 240 healthy common carp fish (52.3 ± 0.9 g) were randomly allocated into four equal groups in triplicate (20 each). The first group left without any zinc sulfate treatment and served as a control group, while the second group through the fourth group were immersed in a zinc sulfate bath at a dose of 2.09, 1.05, and 0.53 mg/L corresponding to 1/5, 1/10, and 1/20 of 96 h LC 50 of Zn, (Zn/5, Zn/10, and Zn/20, respectively). After wound induction, tissue specimens were collected within three different intervals (6 h, 24 h, 72 h, and 14 days). The results indicated that the Zn/5 fish group induced doubled folding increments in the expression of transforming growth factor (TGF)‐β1 after 6 h compared to other groups, whereas collagen type I alpha 1 (COL1α1) and metallothionein (Met) genes exhibited a triple folding increment compared to Zn/10 and a fivefold increase compared to control after two days of wound induction. Moreover, vascular endothelial growth factor (VEGF)‐A and fibroblast growth factor (FGF)‐7 genes showed a dose-dependent manner of expression at all examined points after wound induction. Also, all estimated antioxidant biomarker (superoxide-dismutase, SOD; catalase, CAT; glutathione, GSH; and malonaldehyde, MDA) activities were boosted in the Zn/5 group till three days of wound induction compared to all groups. In addition, the reepithelization score and histological alteration results revealed clear improvement in the Zn/5 group, as most muscle fibers appeared regular, straight, and parallel arranged. In contrast, other groups exhibited a detectable limited area of disrupted muscle fibers. Finally, it could be concluded that the ZnSO 4 immersion bath at 1/5 of the calculated LC 50 effectively enhanced the healing process and skin reepithelization.

This study aims to see if Ginseng® can reduce the hepatorenal damage caused by malathion. Four groups of forty male Wistar albino rats were alienated. Group 1 was a control group that got orally supplied corn oil (vehicle). Group 2 was intoxicated by malathion dissolved in corn oil orally at 135 mg/kg/day. Group 3 orally received both malathion + Panax Ginseng® (300 mg/kg/day). Group 4 was orally given Panax Ginseng® at a 300 mg/kg/day dose. Treatments were administered daily and continued for up to 30 consecutive days. Malathion’s toxic effect on both hepatic and renal tissues was revealed by a considerable loss in body weight and biochemically by a marked increase in liver enzymes, LDH, ACP, cholesterol, and functional renal markers with a marked decrease in serum TP, albumin, and TG levels with decreased AchE and Paraoxonase activity. Additionally, malondialdehydes, nitric oxide (nitrite), 8-hydroxy-2-deoxyguanosine, and TNFα with a significant drop in the antioxidant activities were reported in the malathion group. Malathion upregulated the inflammatory cytokines and apoptotic genes, while Nrf2, Bcl2, and HO-1 were downregulated. Ginseng® and malathion co-treatment reduced malathion’s harmful effects by restoring metabolic indicators, enhancing antioxidant pursuit, lowering the inflammatory reaction, and alleviating pathological alterations. So, Ginseng® may have protective effects against hepatic and renal malathion-induced toxicity on biochemical, antioxidant, molecular, and cell levels.

5-Fluorouracil (5-FU), a chemotherapeutic drug, has adverse effects on heart and kidney functions. Ficus Carica (fig) and extra virgin olive oil (EVOO) are natural sources which have antioxidant effects. This study investigated the synergistic effects of fig extract and EVOO against cardiac and renal damage induced by 5-FU. Forty rats were equally divided into five groups and treated with physiological saline (control), five intravenous injections of 5-FU (40 mg/kg b.w) (5-FU), fig (1 g/kg b.w/day, orally) with 5-FU (Fig/5-FU), EVOO (7 g/kg b.w/day, orally) with 5-FU (EVOO/5-FU), combined treatment of fig and EVOO with five 5-FU injections (Fig/EVOO/5-FU). After 30 days, blood and tissue samples (Heart and kidney) were collected to be used in the examinations. 5-FU significantly increased serum creatine kinase activity, renal biomarkers, cholesterol, triglycerides, C-reactive protein, tumor necrosis factor-α, and interleukin-1β as well as cardiac and renal lipid peroxides (malondialdehyde). Meanwhile, serum levels of immunoglobulins, interleukins (IL-10, IL-12), and antioxidants of heart and kidney tissues were significantly decreased in 5-FU group. It also downregulated cardiac and renal Bcl2, and upregulated cardiac troponin and renin gene expressions. As well, histological alterations clarified that 5-FU induced cardiac cell damage, distorted renal corpuscles and tubules, inflammatory cell infiltrations, and severe congestion and hemorrhage in the blood vessels. The treatment with fig and olive oil, especially the combined treatment, modulated the toxic effect of 5-FU on the heart and kidney. Our results revealed that fig extract and EVOO have a powerful antioxidant and many protective effects against cardiac and renal toxicity induced by 5-FU, especially when using fig and EVOO together as a combined treatment.