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The serum oxidant-antioxidant balance was impaired in children with AD. Serum melatonin levels were higher in children with AD; however, this was negatively correlated with disease severity. Serum NO levels and NO/melatonin and malondialdehyde/melatonin ratios were lower in children with AD than in healthy controls. Melatonin might be used as a promising antioxidant to evaluate disease severity in children with AD. Thus, further studies are needed to clarify the role of melatonin in AD pathogenesis.

Objective: The aim of this article is to measure serum antioxidant melatonin, the oxidants of nitric oxide, and malondialdehyde levels to calculate the serum oxidant–antioxidant balance based on the nitric oxide/melatonin and malondialdehyde/melatonin ratios in children with ADHD. Method: The serum melatonin, nitric oxide, malondialdehyde, and the nitric oxide/melatonin and malondialdehyde/melatonin ratios were calculated and compared between the children with ADHD ( n = 103) and healthy control participants ( n = 73). Results: Serum melatonin and nitric oxide levels were higher, and the nitric oxide/melatonin and malondialdehyde/melatonin ratios were lower in ADHD children than the control group. Melatonin was found to be significantly high, and the malondialdehyde/melatonin ratio was found to be significantly low in children with a positive ADHD family history. Conclusion: The serum oxidant–antioxidant balance was impaired in children with ADHD. Within the ADHD group, higher melatonin levels were determined in the children with a positive family history.

The aim of this study was to investigate the effects of boric acid in experimental acute sciatic nerve injury. Twenty-eight adult male rats were randomly divided into four equal groups (n = 7): control (C), boric acid (BA), sciatic nerve injury (I), and sciatic nerve injury + boric acid treatment (BAI). Sciatic nerve injury was generated using a Yasargil aneurysm clip in the groups I and BAI. Boric acid was given four times at 100 mg/kg to rats in the groups BA and BAI after injury (by gavage at 0, 24, 48 and 72 hours) but no injury was made in the group BA. In vivo electrophysiological tests were performed at the end of the day 4 and sciatic nerve tissue samples were taken for histopathological examination. The amplitude of compound action potential, the nerve conduction velocity and the number of axons were significantly lower and the myelin structure was found to be broken in group I compared with those in groups C and BA. However, the amplitude of the compound action potential, the nerve conduction velocity and the number of axons were significantly greater in group BAI than in group I. Moreover, myelin injury was significantly milder and the intensity of nuclear factor kappa B immunostaining was significantly weaker in group BAI than in group I. The results of this study show that administration of boric acid at 100 mg/kg after sciatic nerve injury in rats markedly reduces myelin and axonal injury and improves the electrophysiological function of injured sciatic nerve possibly through alleviating oxidative stress reactions.

Mesenchymal stem cells can be obtained and multiplied from various sources and have a very high capacity to release exosomes. Exosomes are nano-sized extracellular vesicles containing biological signaling molecules. This study aimed to determine the effect of MSC-derived exosomes as a drug delivery system for paclitaxel in cervical cancer cells. In this study, human MSC were isolated from wharton jelly of umbilical cord tissue (WJ-MSC), and cells were characterized by CD44, CD90, CD105, and CD34 staining. Exosomes were released in WJ-MSC cells with serum-starved conditions for 48 hours, and particle sizes and structures were examined with zeta-sizer and TEM. In addition, exosomes CD9, CD63, and CD81 markers were checked by western blot. Paclitaxel was loaded into exosomes (Exo-PAC) by electroporation and then incubated with Hela cervical cancer cells for 24 hours. TGF-β, SMAD, Snail, Slug, β-catenin, Notch, Caspase-3, Caspase-9, Bax, Bcl-2 protein and gene expression levels were analyzed in Hela cells. As a result, low concentration Exo-PAC induced apoptosis, and suppressed epithelial-mesenchymal transition proteins in Hela cells. In this study, it has been demonstrated that WJ-MSCs can be used as drug delivery systems for cervical cancer if exosomes are produced scalably in the future.

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Objective: Although, the neuroprotective effects of selenium are known, its effect on peripheral nerve injury is not clear. The study was aimed to investigate whether selenium prevents axonal and myelin damage in experimental sciatic nerve injury. Materials and Methods: Twenty-eight male Wistar albino rats were divided into four groups (n=7 in each): control (C), selenium (S), injury (I), and selenium-treated injury (SI). Injury was generated by 30 second of compression via Yasargil aneurysm clip on the sciatic nerve of rats in the I and SI groups. Then, selenium was given to the S and SI groups as 1.5 mg/ kg by oral gavage at 1 st , 24 th , 48 th and 72 nd hour after surgery. According to the experimental protocol, electrophysiological, histological, and biochemical tests were performed end of the day 4. Results: Whereas the amplitude of compound action potential, nerve conduction velocity, average axon diameter, myelin thickness, myelinated/unmyelinated axons and SOD activity in red blood cells of the I group were significantly lower than those of the C, S and SI groups, the serum MDA levels of the I group were significantly higher than those of the C, S and SI groups. Conclusion:The findings of this study show that selenium decreases axonal and myelin damage after sciatic nerve injury and that this neuroprotective effect of selenium is at least partially mediated by oxidant/antioxidant mechanisms.