9 research outputs found

    The role of melatonin and carnosine in prevention of oxidative intestinal injury induced by gamma irradiation in rats

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    Exposure of biological materials to ionizing irradiation causes accumulation of reactive oxygen species. The current study aimed to investigate whether melatonin or carnosine could provide protection against irradiation-induced small intestinal damage. FortyWistar albino rats were divided into five groups. Melatonin, carnosine, and combination of carnosine and melatonin were injected into rats in the third, fourth, and fifth groups, respectively. Rats were injected three times every 48 hours. All groups, excluding the control group, were exposed to a dose of 8 Gray whole body gamma irradiation one hour after the second injection. It was determined that irradiation caused degenerative changes in the intestinal tissues, reduced PCNA (proliferating cell nuclear antigen) - positive cell number, and increased caspase-3 and TNF-alpha (tumour necrosis factor alpha) - positive crypt cell numbers. Results obtained from antioxidant-treated groups were similar to those from the control group. Lipid peroxidation and protein carbonyl levels as well as superoxide dismutase, glutathione peroxidase, glutathioneS- transferase, myeloperoxidase, lactate dehydrogenase and xanthine oxidase activities were increased. However, catalase, sodium potassium ATPase activities and glutathione levels were decreased in the irradiated group of animals. Treatment with antioxidants reversed these changes. It is suggested that exogenous melatonin, carnosine, and melatonin+carnosine combination exhibit protective effects against irradiation-induced small intestinal damage

    Role of Exogenous Melatonin on Cell Proliferation and Oxidant/Antioxidant System in Aluminum-Induced Renal Toxicity

    No full text
    Aluminum has toxic potential on humans and animals when it accumulates in various tissues. It was shown in a number of studies that aluminum causes oxidative stress by free radical formation and lipid peroxidation in tissues and thus may cause damage in target organs. Although there are numerous studies investigating aluminum toxicity, biochemical mechanisms of the damage caused by aluminum have yet to be explained. Melatonin produced by pineal gland was shown to be an effective antioxidant. Since kidneys are target organs for aluminum accumulation and toxicity, we have studied the role of melatonin against aluminum-induced renal toxicity in rats. Wistar albino rats were divided into five groups. Group I served as control, and received only physiological saline; group II served as positive control for melatonin, and received ethanol and physiological saline; group III received melatonin (10 mg/kg); group IV received aluminum sulfate (5 mg/kg) and group V received aluminum sulfate and melatonin (in the same dose), injected three times a week for 1 month. Administration of aluminum caused degenerative changes in renal tissues, such as increase in metallothionein immunoreactivity and decrease in cell proliferation. Moreover, uric acid and lipid peroxidation levels and xanthine oxidase activity increased, while glutathione, catalase, superoxide dismutase, paraoxonase 1, glucose-6-phosphate dehydrogenase, and sodium potassium ATPase activities decreased. Administration of melatonin mostly prevented these symptoms. Results showed that melatonin is a potential beneficial agent for reducing damage in aluminum-induced renal toxicity

    Cytogenetic and Molecular Investigation in Children with Possible Fragile X Syndrome

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    Objective: Fragile X syndrome (FXS) is the most common cause of inherited mental retardation and is due to a mutation in the X-linked FMR1 gene. Molecular genetic testing and chromosome analysis are indicated for this disorder. In this context, we tried to determine the frequency of the FXS, and other chro¬mosomal abnormalities of Turkish pediatric neurology outpatients. Materials and Methods: Cytogenetic and molecular screenings were performed to esti-mate the prevalence of the fragile X in 107 patients with mental retardation, language disorders, hyperactivity, develop¬mental delay or fragile X syndrome phenotype. Only 26 out of 107 patients were screened, molecularly. Results: Cytogenetically fragile X-positive cells was found in 8 cases (7.5%) of 107 patients; in 4.7% of males and in 2.8% of females. The autosomal fragile sites (FS) was found in 14 (13.1%) cases. One (0.9%) patient had pericentric inversion of chromosome 9. Molecular analysis were performed for 26 patients and all patients showed normal CGG expansion. Conclusion: In diagnosis of fragile X syndrome, chromosome analysis must be run in conjunction with the molecular studies. It is recommended that all members of the fragile X family under risk should be screened both by cytogenetic and molecular methods. Genetic counseling can be useful to patients and families considering genetic testing. [Cukurova Med J 2012; 37(2.000): 76-83

    Prevalence, etiology, and biopsychosocial risk factors of cervicogenic dizziness in patients with neck pain: A multi-center, cross-sectional study

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    Objectives: This study aims to investigate the prevalence, etiology, and risk factors of cervicogenic dizziness in patients with neck pain. Patients and methods: Between June 2016 and April 2018, a total of 2,361 patients (526 males, 1,835 females; mean age: 45.0 +/- 13.3 years; range, 18 to 75 years) who presented with the complaint of neck pain lasting for at least one month were included in this prospective, cross-sectional study. Data including concomitant dizziness, severity, and quality of life (QoL) impact of vertigo (via Numeric Dizziness Scale [NDS]), QoL (via Dizziness Handicap Inventory [DHI]), mobility (via Timed Up-and-Go [TUG] test), balance performance [via Berg Balance Scale [BBS]), and emotional status (via Hospital Anxiety Depression Scale [HADS]) were recorded. Results: Dizziness was evident in 40.1% of the patients. Myofascial pain syndrome (MPS) was the most common etiology for neck pain (58.5%) and accompanied with cervicogenic dizziness in 59.7% of the patients. Female versus male sex (odds ratio [OR]: 1.641, 95% CI: 1.241 to 2.171, p=0.001), housewifery versus other occupations (OR: 1.285, 95% CI: 1.006 to 1.642, p=0.045), and lower versus higher education (OR: 1.649-2.564, p<0.001) significantly predicted the increased risk of dizziness in neck pain patients. Patient with dizziness due to MPS had lower dizziness severity scores (p=0.034) and milder impact of dizziness on QoL (p=0.005), lower DHI scores (p=0.004), shorter time to complete the TUG test (p=0.001) and higher BBS scores (p=0.001). Conclusion: Our findings suggest a significant impact of biopsychosocial factors on the likelihood and severity of dizziness and association of dizziness due to MPS with better clinical status

    Role of Exogenous Melatonin on Cell Proliferation and Oxidant/Antioxidant System in Aluminum-Induced Renal Toxicity

    No full text
    Aluminum has toxic potential on humans and animals when it accumulates in various tissues. It was shown in a number of studies that aluminum causes oxidative stress by free radical formation and lipid peroxidation in tissues and thus may cause damage in target organs. Although there are numerous studies investigating aluminum toxicity, biochemical mechanisms of the damage caused by aluminum have yet to be explained. Melatonin produced by pineal gland was shown to be an effective antioxidant. Since kidneys are target organs for aluminum accumulation and toxicity, we have studied the role of melatonin against aluminum-induced renal toxicity in rats. Wistar albino rats were divided into five groups. Group I served as control, and received only physiological saline; group II served as positive control for melatonin, and received ethanol and physiological saline; group III received melatonin (10 mg/kg); group IV received aluminum sulfate (5 mg/kg) and group V received aluminum sulfate and melatonin (in the same dose), injected three times a week for 1 month. Administration of aluminum caused degenerative changes in renal tissues, such as increase in metallothionein immunoreactivity and decrease in cell proliferation. Moreover, uric acid and lipid peroxidation levels and xanthine oxidase activity increased, while glutathione, catalase, superoxide dismutase, paraoxonase 1, glucose-6-phosphate dehydrogenase, and sodium potassium ATPase activities decreased. Administration of melatonin mostly prevented these symptoms. Results showed that melatonin is a potential beneficial agent for reducing damage in aluminum-induced renal toxicity
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