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The present investigation explored the potential neuroprotective role of zinc oxide nanoparticles (ZnONPs) on aluminum chloride (AlCl 3 )-mediated Alzheimer's disease (AD)-like symptoms. Rats were distributed into four treatment groups equally: control, ZnONPs (4 mg/kg b.wt.), AlCl 3 (100 mg/kg b.wt.), and ZnONPs + AlCl 3 groups. Rats were treated for 42 consecutive days. ZnONPs injection into AlCl 3 -treated rats suppressed the development of oxidative challenge in the cortical and hippocampal tissues, as demonstrated by the decreased neuronal pro-oxidants (malondialdehyde and nitric oxide), and the increased glutathione and catalase levels. Additionally, ZnONPs injection showed anti-inflammatory potency in response to AlCl 3 by decreasing levels of tumor necrosis factor-α and interleukin-1β. Moreover, pretreatment with ZnONPs prevented neuronal cell loss by decreasing the level of pro-apoptotic caspase-3 and enhancing the anti-apoptotic B cell lymphoma 2. Furthermore, ZnONPs ameliorated the disturbed acetylcholinesterase activity, monoamines (norepinephrine, dopamine, and serotonin), excitatory (glutamic and aspartic acids), and inhibitory amino acids (GABA and glycine) in response to AlCl 3 exposure. These findings indicate that ZnONPs may have the potential as an alternative therapy to minimize or prevent the neurological deficits in AD model by exhibiting antioxidative, anti-inflammation, anti-apoptosis, and neuromodulatory effects., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Reproductive toxicity is a major challenge associated with aluminum (Al) exposure. Therefore, this study aimed to investigate the effects of zinc oxide nanoparticle (ZnONP) treatment on Al-induced reproductive toxicity in rats. Thirty-two adult male albino rats were allocated into four equal groups as follows: control, AlCl 3 orally administered group (100 mg/kg bwt), ZnONPs injected intraperitoneally (i.p.) group (4 mg/kg bwt), and ZnONPs + AlCl 3 -treated group. The treatment was daily extended for 42 consecutive days. Oral administration of AlCl 3 showed an oxidative damage confirmed by an increase in malondialdehyde and nitric oxide levels and superoxide dismutase activity and accompanied by a decrease in glutathione content and catalase activity. Also, AlCl 3 administration increased the pro-inflammatory mediator tumor necrosis factor-alpha. Furthermore, significant declines in the levels of serum male reproductive hormones testosterone, luteinizing hormone, and follicle-stimulating hormone in AlCl 3 -intoxicated rats were noticed. In parallel, severe histopathological alterations were observed in testis tissues. Additionally, the immunohistochemical analysis showed that AlCl 3 administration potentiates cell death in the testicular tissue by elevating the immunostaining intensity signal for the pro-apoptotic protein, cysteinyl aspartate specific protease-3 (caspase-3) and a marked depletion in the cell proliferation expression marker, Ki-67, in germinal cells of AlCl 3 -treated group. On the other hand, the daily i.p. injection to rats with ZnONPs before AlCl 3 was found to ameliorate the reproductive toxicity induced by Al administration through reducing the testicular oxidative stress and improving the inflammatory, apoptotic, and reproductive markers as well as histopathological alterations in the testis. These results suggest that ZnONPs could be used as an alternative agent to minimize the reproductive toxicity associated with Al exposure through its antioxidant, anti-inflammatory, anti-apoptotic, and reproductive modulatory activities., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Chlorpyrifos (CPF) is a widely used organophosphate insecticide with several harmful effects. N-acetylcysteine (NAC) represents an ideal antixenobiotic; it can directly enter endogenous biochemical processes and is used as adjunctive treatment for psychiatric disorders. We aimed to evaluate the neuroprotective effect of NAC as an antioxidant drug against CPF-induced neurotoxicity in adult male albino rat brains. Twenty-eight male Wister rats were allocated into four groups (n = 7) and were administered the following for 28 days: group I (control group), physiological saline (0.9% NaCl); group II (CPF group), 10 mg/kg body weight (BW) CPF; group III (NAC group), 100 mg/kg BW NAC; and group VI (CPF+NAC group), NAC 1 h before CPF. CPF intoxication resulted in acetylcholinesterase inhibition, reduced glutathione content, and elevated levels of malondialdehyde and nitric oxide, which are oxidative stress biomarkers. CPF also depleted the activity of antioxidant enzymes, superoxide dismutase and catalase, and levels of inflammatory mediators, tumor necrosis factor-α, interleukin (IL)-6, and IL-1β. Levels of vascular endothelial growth factor, Bax, and the proapoptotic caspases-3 also increased, while brain-derived neurotrophic factor level decreased. Additionally, CPF significantly diminished Bcl-2 (an antiapoptotic protein) in rat brain cortical tissue. NAC treatment was found to protect brain tissue by reversing the CPF-induced neurotoxicity. Our results show the antioxidant, antiinflammatory, and antiapoptotic effects of NAC on CPF-induced neurotoxicity in rat brain tissue.

Graphene and graphene-related materials have broadly applied in biomedical purposes due to their unique properties, thus safety evaluation of them is crucial. This study was performed to explore the genotoxic and pulmonary toxic potential of different doses of graphene oxide nanosheets' (GOs) in mice.A total of 90 male mature mice were randomly divided into six groups of fifteen mice per each, five groups were intraperitoneally injected by GO at doses of 10, 50, 100, 250 and 500μg/kg b.w once weekly in addition to the control group that was injected intraperitoneally with 0.2ml saline solution. Five animals from each group were euthanized after 7, 28 and 56days post treatment. Evaluation of genotoxicity was performed through detection of chromosomal aberrations in bone marrow while assessment of lung injury was made by determination of DNA fragmentation in lung specimens using the alkali Comet assay, pulmonary oxidative markers estimation and finally histopathological investigations. Results revealed that GOs induced variable structural chromosomal aberrations (SCA) in bone marrow and DNA damage of lung cells that were time and dose dependent and represented by increase in%DNA in comet tail, tail moment and tail length and decrease in% head DNA in nuclei of lung of GOs-treated mice versus control groups in addition, GOs induced various changes in pulmonary oxidative stress parameters that were affected by dose and duration of treatment compared with the control as well as various pulmonary histopathological alterations were detected indicating lung injury., Conclusion: GO potentiate the induction of genotoxicity and pulmonary injury in mice in time and dose dependent manner., (Copyright © 2017 Elsevier GmbH. All rights reserved.)

Development of the amphibian vestibular organ is regulated by molecular and neuronal mechanisms and by environmental input. The molecular component includes inductive signals derived from neural tissue of the hindbrain and from the surrounding mesoderm. The integrity of hindbrain patterning, on the other hand, depends on instructive signals from the isthmus organizer of the midbrain, including the transcription factor XTcf-4. If the development of the vestibular system depends on the integrity of the isthmus as the organizing centre, suppression of isthmus maintenance should modify vestibular morphology and function. We tested this hypothesis by downregulation of the transcription factor XTcf-4. 10 pmol l(-1) XTcf-4-specific antisense morpholino oligonucleotide was injected in one blastomere of two-cell-stage embryos of Xenopus laevis. For reconstitution experiments, 500 pg mRNA of the repressing XTcf-4A isoform or the activating XTcf-4C isoform were co-injected. Overexpression experiments were included using the same isoforms. Otoconia formation and vestibular controlled behaviour such as the roll-induced vestibuloocular reflex (rVOR) and swimming were recorded two weeks later. In 50% of tadpoles, downregulation of XTcf-4 induced (1) a depression of otoconia formation accompanied by a reduction of the rVOR, (2) abnormal tail development and (3) loop swimming behaviour. (4) All effects were rescued by co-injection of XTcf-4C but not, or only partially, by XTcf-4A. (5) Overexpression of XTcf-4A caused similar morphological and rVOR modifications as XTcf-4 depletion, while overexpression of XTcf-4C had no effect. Because XTcf-4C has been described as an essential factor for isthmus development, we postulate that the isthmus is strongly involved in vestibular development.