Agomelatine could prevent brain and cerebellum injury against LPS-induced neuroinflammation in rats.

Sepsis, systemic hyper-inflammatory immune response, causes the increase of morbidity and mortality rates due to multi-organ diseases such as neurotoxicity. Lipopolysaccharide (LPS) induces inflammation, oxidative stress and apoptosis to cause brain damage. We aimed to evaluate the antioxidant, anti-inflammatory and antiapoptotic effects of Agomelatine (AGM) on LPS induced brain damage via NF-kB signaling. Twenty-four animals were divided into three groups as control, LPS (5 mg/kg) and LPS + AGM (20 mg/kg). Six hours after the all administrations, rats were sacrificed, brain tissues were collected for biochemical, histopathological and immunohistochemical analysis. In LPS group; total oxidant status (TOS), OSI index, Caspase-8 (Cas-8), NF-kß levels increased and Total antioxidant status (TAS) levels decreased biochemically and Cas-8, haptoglobin and IL-10 expressions increased and sirtuin-1 (SIRT-1) levels decreased immunohistochemically. AGM treatment reversed these parameters except haptoglobin levels in hippocampus and SIRT-1 levels in cerebellum. Besides, AGM treatment blocked the phosphorylation of NF-kB biochemically and ameliorated increased the levels of hyperemia, edema and degenerative changes histopathologically. In conclusion, AGM enhanced SIRT-1 levels to negatively regulate the transcription and activation of p-NF-kB/p65 which caused to ameliorate inflammation, oxidative stress and apoptosis.

TP53 polymorphisms in smokers' and nonsmokers' pericoronal follicles of asymptomatic impacted third molars.

BACKGROUND AND PURPOSE: The investigators designed and implemented a prospective cohort study composed of smoking and nonsmoking patients with asymptomatic fully impacted mandibular third molars. The objective of the paper was to evaluate 21 single-nucleotide polymorphisms (SNP) on the TP53 gene in smokers' (S) and nonsmokers' (NS) pericoronal follicles of asymptomatic impacted third molars. MATERIALS AND METHODS: Matrix-assisted desorption/ionization time of the flight mass spectrometry was used for SNP analysis of 21 regions in the TP53 gene. Descriptive statistics and Chi-square tests were computed with a P value of 0.05. RESULTS: : Ten of the 21 SNPs related to oral pathologies according to NCBI dbSNP, were detected; in these, the genotypic frequencies showed no differences between the S and NS groups (P > 0.05). The results showed a high ratio of SNPs without correlation between smoking and TP53 gene status. CONCLUSION: Further studies should examine the entire TP53 gene to elucidate how smoking affects it in larger study populations.

Oral mucosa and lung cancer: Are genetic changes in the oral epithelium associated with lung cancer?

AIM: To compare genetic aberrations in the oral epithelium of lung cancer patients with those without cancer. SUBJECTS AND METHODS: Buccal smears were performed to collect oral epithelium from each of the participants (smoker cancer patients n = 50, smoker control subjects n = 40, and nonsmoker control subjects n = 25). Cytogenetic changes in the samples were detected by micronuclei assay, whereas p53 and murine double minute 2 (MDM2) polymorphisms were genotyped using polymerase chain reaction-restriction fragment length polymorphism. RESULTS: p53 codon 72 polymorphism was seen in 44% of cancer patients versus 12.5% in smokers and 12% in nonsmokers of the control group. Similarly, MDM2 single nucleotide polymorphism 309 polymorphism was seen in 34% of patients with lung cancer as opposed to 12.5% of smokers (P = 0.038) and 8% of nonsmokers (P = 0.019) of the control group. CONCLUSION: A higher proportion of individuals with lung cancer demonstrate genetic damage to oral mucosa compared to those without cancer.

Cytogenetic findings in patients diagnosed with breast cancer having undergone adjuvant chemotherapy regimens.

The aim of the present study was to investigate DNA damage in peripheral blood lymphocytes of breast cancer (BC) patients before and after administration of chemotherapy. We analyzed the frequency of sister chromatid exchange (SCE), occurrence of micronuclei (MN), and lymphocyte proliferation rate index (PRI) as cytogenetic markers in 28 female BC patients before and after chemotherapy, and in 20 age-matched healthy female volunteers. Prior to treatment, BC patients showed significantly increased background levels of SCE and MN, and lowered PRIs compared to healthy women. In comparison with pre-treatment levels, SCE and MN frequencies were significantly elevated and PRI reduced in blood samples collected after chemotherapy. Our findings indicate that SCE, MN, and PRI may serve as sensitive biomarkers for routine detection of the genetic abnormalities that may occur following administration of antineoplastic drugs in the clinical setting, as well as for the monitoring of high-risk patients receiving chemotherapy for BC.

Protective effects of melatonin against oxidative injury in rat testis induced by wireless (2.45 GHz) devices.

Wireless devices have become part of everyday life and mostly located near reproductive organs while they are in use. The present study was designed to determine the possible protective effects of melatonin on oxidative stress-dependent testis injury induced by 2.45-GHz electromagnetic radiation (EMR). Thirty-two rats were equally divided into four different groups, namely cage control (A1), sham control (A2), 2.45-GHz EMR (B) and 2.45-GHz EMR+melatonin (C). Group B and C were exposed to 2.45-GHz EMR during 60 min day(-1) for 30 days. Lipid peroxidation levels were higher in Group B than in Group A1 and A2. Melatonin treatment prevented the increase in the lipid peroxidation induced by EMR. Also reduced glutathione (GSH) and glutathione peroxidase (GSH-Px) levels in Group D were higher than that of exposure group. Vitamin A and E concentrations decreased in exposure group, and melatonin prevented the decrease in vitamin E levels. In conclusion, wireless (2.45 GHz) EMR caused oxidative damage in testis by increasing the levels of lipid peroxidation and decreasing in vitamin A and E levels. Melatonin supplementation prevented oxidative damage induced by EMR and also supported the antioxidant redox system in the testis.