a b s t r a c tArsenic is a neurotoxic substance that makes the brain susceptible to free radicals. Thymoquinone (TQ) is a potent antioxidant extracted from Nigella sativa seeds. It scavenges free radicals and prevents the cell damage resulted from oxidative substances. In this study, the ameliorative effect of TQ in arsenic-induced neurotoxicity was investigated. Rats were treated for 21 days with: distilled water, 20 mg/kg sodium arsenate, 10 mg/kg TQ, and arsenate followed by TQ. Cerebral cortex, cerebellum and brain stem were removed for the measurements of different physiological parameters. Cerebelli were prepared for histopathological studies. Arsenate treatment caused a decrease in the levels of norepinephrine (NE), dopamine (DA), acetylcholine esterase (AChE) and Na + -K + -ATPase activities in cerebral cortex, cerebellum, and brain stem of rats. Similarly, the levels of glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD), catalase (CAT) were declined. In contrast, serotonin (5-HT), lipid peroxidation (MDA), nitrite/nitrate (NO), and tumour necrosis factor (TNF-a) levels were increased after arsenate treatment. The presence of degenerated Purkinje cells in cerebellum was noticed. Results revealed that, post-treatment with TQ suppressed the arsenate-induced neurotoxic effects as it decreased the levels of 5-HT, MAD, NO, TNF-a and increased the levels of NE, DA, GH, GPx, GR, SOD, and CAT, in the cerebral cortex, cerebellum, and brain stem. Likewise, AChE and Na + -K + -ATPase activities were increased after TQ post-treatment. In conclusion, TQ ameliorated the neurotoxic effect of arsenate and suppressed the oxidative stress induced in the nervous system through its antioxidant mechanism. Ó 2017 Mansoura University. Production and hosting by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

In mammals, the principal circadian clock within the suprachiasmatic nucleus (SCN) entrains the phase of clocks in numerous peripheral tissues and controls the rhythmicity in various body functions. During ontogenesis, the molecular mechanism responsible for generating circadian rhythmicity develops gradually from the prenatal to the postnatal period. In the beginning, the maternal signals set the phase of the newly developing fetal and early postnatal clocks, whereas the external light-dark cycle starts to entrain the clocks only later. This minireview discusses the complexity of signaling pathways from mothers and the outside world to the fetal and newborn animals' circadian clocks.

Respiratory infections by bacteria of the Burkholderia cepacia complex (Bcc) remain an important cause of morbidity and mortality among cystic fibrosis patients, highlighting the need for novel therapeutic strategies. In the present work we have studied the B. cenocepacia protein BCAL2958, a member of the OmpA-like family of proteins, demonstrated as highly immunogenic in other pathogens and capable of eliciting strong host immune responses. The encoding gene was cloned and the protein, produced as a 6× His-tagged derivative, was used to produce polyclonal antibodies. Bioinformatics analyses led to the identification of sequences encoding proteins with a similarity higher than 96 % to BCAL2958 in all the publicly available Bcc genomes. Furthermore, using the antibody it was experimentally demonstrated that this protein is produced by all the 12 analyzed strains from 7 Bcc species. In addition, results are also presented showing the presence of anti-BCAL2958 antibodies in sera from cystic fibrosis patients with a clinical record of respiratory infection by Bcc, and the ability of the purified protein to in vitro stimulate neutrophils. The widespread production of the protein by Bcc members, together with its ability to stimulate the immune system and the detection of circulating antibodies in patients with a documented record of Bcc infection strongly suggest that the protein is a potential candidate for usage in preventive therapies of infections by Bcc.

Exposure to lead (Pb) causes multiorgan dysfunction including reproductive impairments. Here, we examined the protective effects of coenzyme Q10 (CoQ10) administration on testicular injury induced by lead acetate (PbAc) exposure in rats. This study employed four experimental groups (n=7) that underwent seven days of treatment as follows: control group intraperitoneally (i.p.) treated with 0.1 ml of 0.9% NaCl containing 1% Tween 80 (v:v), CoQ10 group that was i.p. injected with 10 mg/kg CoQ10, PbAc group that was i.p. treated with PbAc (20 mg/kg), and PbAc+CoQ10 group that was i.p. injected with CoQ10 2 h after PbAc. PbAc injection resulted in increasing residual Pb levels in the testis and reducing testosterone, luteinizing hormone, and follicle-stimulating hormone levels. Additionally, PbAc exposure resulted in significant oxidative damage to the tissues on the testes. PbAc raised the levels of prooxidants (malondialdehyde and nitric oxide) and reduced the amount of endogenous antioxidative proteins (glutathione and its derivative enzymes, catalase, and superoxide dismutase) available in the cell. Moreover, PbAc induced the inflammatory response as evidenced by the upregulation of inflammatory mediators (tumor necrosis factor-alpha and interleukin-1 beta). Further, PbAc treatment induced apoptosis in the testicular cells, as indicated by an increase in Bax and caspase 3 expression, and reduced Bcl2 expression. CoQ10 supplementation improved testicular function by inhibiting Pb accumulation, oxidative stress, inflammation, cell death, and histopathological changes following PbAc exposure. Our findings suggest that CoQ10 can act as a natural therapeutic agent to protect against the reproductive impairments associated with PbAc exposure.