Peripheral blood cultures were exposed to various doses (5 to 500 mg/L) of boron compounds. Sister-chromatid exchange, micronucleus and chromosomal aberration tests were applied to estimate the DNA damage, and biochemical parameters (superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, glucose-6-phosphate dehydrogenase, total glutathione, malondialdehyde and total antioxidant capacity) were examined to determine oxidative stress. According to our findings, various boron compounds at low doses were useful in supporting antioxidant enzyme activities in human blood cultures. It was found that the boron compounds do not have genotoxic effects even in the highest concentrations, though in increasing doses they constitute oxidative stress. It is concluded that the tested boron compounds can be used safely, but it is necessary to consider the tissue damages which are likely to appear depending on the oxidative stress.

Introduction: Oxidative stress may contribute to the pathogenesis of periodontitis. However, the detailed molecular mechanism remains unclear. Both 8-hydroxydeoxyguanosine (8-OHdG) and mitochondrial DNA (mtDNA) deletion have been reported as early oxidative DNA damage markers. In this study, 8-OHdG levels in saliva and mtDNA deletions in gingival tissue of patients with chronic periodontitis (CP) were evaluated. Materials and Methods: Gingival tissue and whole saliva samples were collected from 32 patients with CP and 32 healthy control subjects. To determine the clinical condition of each subject, the plaque index, gingival index, clinical attachment level (CAL), and probing depth (PD) were measured. Using the ELISA and polymerase chain reaction methods, the salivary 8-OHdG levels and the 7.4-kbp and 5-kbp mtDNA deletions were examined. Results: The 5-kbp mtDNA deletion was detected in 20 of the 32 periodontitis patients (62.5%), but was not detected in the healthy controls. The mean value of 8-OHdG in the saliva of the periodontitis patients with deleted mtDNA was significantly higher than in the patients with non-deleted mtDNA (p<0.01). Also, significant correlation was found between the occurrence of the 5-kbp mtDNA deletion and salivary 8-OHdG levels (p<0.01). Similar correlations were detected between salivary 8-OHdG levels and age, PD, and CAL (p<0.01, p<0.05). Conclusion: Increased oxidative stress may lead to premature oxidative DNA damage in the gingival tissue of periodontitis patients and the salivary 8-OHdG level may signify premature oxidative mtDNA damage in diseased gingival tissue.

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Paclitaxel (PAC) and cisplatin (CIS) are two established chemotherapeutic drugs used in combination for the treatment of various solid tumors. However, the usage of PAC and CIS are limited because of the incidence of their moderate or severe neurotoxic side effects. In this study, we aimed to assess the protective role of salicylic acid (SA) against neurotoxicity caused by PAC and CIS. For this purpose, newborn Sprague Dawley rats were decapitated in sterile atmosphere and primary cortex neuron cultures were established. On the 10th day SA was added into culture plates. PAC and CIS were added on the 12th day. The cytotoxicity was determined by using the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay. Oxidative alterations were assessed using total antioxidant capacity and total oxidative stress assays in rat primary neuron cell cultures. It was shown that both concentrations of PAC and CIS treatments caused neurotoxicity. Although SA decreased the neurotoxicity by CIS and PAC, it was more effective against the toxicity caused by CIS rather than the toxicity caused by PAC. In conclusion it was clearly revealed that SA decreased the neurotoxic effect of CIS and PAC in vitro.

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Nanotechnology is increasingly developing area including more than 700 commercial products such as clothing, food preparation, cosmetics, mechanics, electronics and also health industry. People generally contact with nanoparticles by inhaling from air. Thus, it is becoming important issue to understand harmful effects of nanoparticles on human health and prepare risk reports for common nano-sized materials. In this paper, synthesis, characterization and cytotoxicity evaluation of boron nitride (BN) nanoparticles were performed on human primary alveolar epithelial cells (HPAEpiC) since, main exposure to nanoparticles would generally happen through lung via inhalation. Chemically synthetized BN nanoparticles were characterized by using X-ray crystallography, transmission electron microscope, scanning

Two sisters presented with partial alopecia, primary hypergonadotropic hypogonadism and Mullerian hypoplasia associated with mild mental retardation, microcephaly, flat occiput, sparse eyebrows, absence of breast tissue, absent ovaries, mild-moderate dorsal kyphosis, thin upper lip and unilateral sensorioneural deafness in one of them. They were the product of a Turkish consanguineous marriage. The clinical course for our patients is similar to two families reported by Al-Awadi et al. [Al-Awadi et al. (1985) Am J Med Genet 22:619-622] and Megarbane et al. [Megarbane et al. (2003) Am J Med Genet Part A 119A:214-217]. This report supports the literature by proposing an autosomal recessive syndrome which was firstly reported by Al-Awadi et al. [Al-Awadi et al. (1985) Am J Med Genet 22:619-622]. This condition may be due to a founder mutation.

Oxidative stress is highly damaging to cellular macromolecules and is also considered a main cause of the loss and impairment of neurons in several neurodegenerative disorders. Recent reports indicate that farnesene (FNS), an acyclic sesquiterpene, has antioxidant properties. However, little is known about the effects of FNS on oxidative stress-induced neurotoxicity. We used hydrogen peroxide (H2O2) exposure for 6 h to model oxidative stress. Therefore, this experimental design allowed us to explore the neuroprotective potential of different FNS isomers (α-FNS and β-FNS) and their mixture (Mix-FNS) in H2O2-induced toxicity in newborn rat cerebral cortex cell cultures for the first time. For this aim, both MTT and lactate dehydrogenase assays were carried out to evaluate cell viability. Total antioxidant capacity (TAC) and total oxidative stress (TOS) parameters were used to assess oxidative alterations. In addition to determining of 8-hydroxy-2-deoxyguanosine (8-OH-dG) levels in vitro, the comet assay was also performed for measuring the resistance of neuronal DNA to H2O2-induced challenge. Our results showed that survival and TAC levels of the cells decreased, while TOS, 8-OH-dG levels and the mean values of the total scores of cells showing DNA damage (comet assay) increased in the group treated with H2O2 alone. But pretreatment of FNS suppressed the cytotoxicity, genotoxicity and oxidative stress, which were increased by H2O2 in clear type of isomers and applied concentration-dependent manners. The order of antioxidant effectiveness for modulating H2O2-induced oxidative stress-based neurotoxicity and genotoxicity is as β-FNS > Mix-FNS > α-FNS.