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1.
Ren Fail ; 38(1): 117-23, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-26513487

RESUMO

We aimed to investigate the protective role of thymoquinone (TQ) by targeting its antiapoptotic and antioxidant properties against kidney damage induced by arsenic in rats. We have used the 24 male Sprague-Dawley rats. Rats were divided into three groups. Physiological serum in 10 mL/kg dose as intragastric was given to the control group. Sodium arsenite (10 mg/kg, intragastric by gavage for fifteen days) was given to the arsenic group. Sodium arsenite (10 mg/kg, intragastric by gavage for fifteen days) and TQ (10 mg/kg, intragastric by gavage for 15 days) was given to the arsenic + TQ group. After 15 days, the animals' kidneys were taken theirs, then we have performed histological and apoptotic assessment. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzyme activities and malondialdehyde (MDA) levels have examined as the oxidative stress parameters. We have determined the levels of arsenic. Increased renal injury and apoptotic cells have been detected in the arsenic group. Degenerative changes in the arsenic + TQ group were diminished. Although the MDA levels were augmented in the arsenic group, SOD, CAT and GSH-Px enzyme activities were lessened than the other groups. Our findings suggest that TQ may impede the oxidative stress, the cells have been damaged and also the generation of apoptotic cells arisen from arsenic. TQ plays a protective role against arsenic-induced toxicity in kidney and may potentially be used as a remedial agent.


Assuntos
Apoptose/efeitos dos fármacos , Intoxicação por Arsênico/complicações , Benzoquinonas/uso terapêutico , Nefropatias/prevenção & controle , Estresse Oxidativo/efeitos dos fármacos , Animais , Antioxidantes/metabolismo , Arsênio/metabolismo , Intoxicação por Arsênico/enzimologia , Intoxicação por Arsênico/patologia , Benzoquinonas/farmacologia , Avaliação Pré-Clínica de Medicamentos , Rim/enzimologia , Rim/patologia , Nefropatias/induzido quimicamente , Nefropatias/enzimologia , Nefropatias/patologia , Masculino , Malondialdeído/metabolismo , Ratos Sprague-Dawley
2.
Neuropharmacology ; 49(4): 456-64, 2005 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-15913671

RESUMO

Nigella sativa oil (NSO), a herbaceous plant, has been used for thousands of years for culinary and medical purposes. This study aimed to investigate the anticonvulsant and antioxidant activities of NSO on pentylenetetrazol (PTZ) kindling seizures in mice. Nigella sativa oil was tested for its ability (i) to suppress the convulsive and lethal effects of PTZ in kindled mice (anti-epileptogenic effect), (ii) to attenuate the PTZ-induced oxidative injury in the brain tissue (antioxidant effect) when given as a pretreatment prior to each PTZ injection during kindling acquisition. Valproate, a major antiepileptic drug, was also tested for comparison. Both substances studied significantly decreased oxidative injury in the mouse brain tissue in comparison with the PTZ-kindling group. Nigella sativa oil was found to be the most effective in preventing PTZ-induced seizures relative to valproate. Nigella sativa oil showed anti-epileptogenic properties as it reduced the sensitivity of kindled mice to the convulsive and lethal effects of PTZ; valproate was ineffective in preventing development of any of these effects. The data obtained support the hypothesis that neuroprotective action of NSO may correlate with its ability to inhibit not only excessive reactive oxygen species (ROS) formation but also seizure generation.


Assuntos
Anticonvulsivantes/uso terapêutico , Antioxidantes/uso terapêutico , Excitação Neurológica/efeitos dos fármacos , Óleos de Plantas/uso terapêutico , Convulsões/tratamento farmacológico , Adenosina Desaminase/metabolismo , Análise de Variância , Animais , Relação Dose-Resposta a Droga , Interações Medicamentosas , Glutationa Peroxidase/metabolismo , Masculino , Malondialdeído/metabolismo , Camundongos , Óxido Nítrico/metabolismo , Pentilenotetrazol , Convulsões/induzido quimicamente , Convulsões/embriologia , Fatores de Tempo , Ácido Valproico/uso terapêutico , Xantina Oxidase/metabolismo
3.
J Chem Neuroanat ; 29(3): 173-8, 2005 May.
Artigo em Inglês | MEDLINE | ID: mdl-15820619

RESUMO

Formaldehyde (FA) can cause severe central nervous system impairment. But, there are only a few studies about biochemical and histopathological changes of frontal cortex and hippocampal tissue caused by FA toxicity. The aim of our study was to investigate these changes occurring after chronic formaldehyde toxicity in frontal cortex and hippocampal tissues, and protective effect of Vitamin E (vit E) against oxidative damage. Eighteen rats were divided into three groups: (1) control, (2) treated with FA (FAt), and (3) treated with FA and vit E (FAt+vit E) groups. After the treatment, the animals were sacrificed and frontal cortex and hippocampal tissues were removed for biochemical and histopathological investigation. FA significantly increased tissue malondialdehyde (MDA) and protein carbonyl (PC) levels and also decreased superoxide dismutase (SOD) and catalase (CAT) enzyme activities in frontal cortex and hippocampal tissue compared to control. Vit E treatment decreased MDA and PC levels and prevented inhibition of SOD and CAT enzymes in the tissues. In the FAt group, the neurons of both tissues became extensively dark and degenerated with picnotic nuclei. The morphology of neurons in FAt+vit E group was protected well, but not as neurons of the control group. The number of neurons in frontal cortex and hippocampal tissue of FAt group was significantly less than both control and FAt+vit E groups. It was concluded that vit E treatment might be beneficial in preventing FA-induced oxidative frontal cortex and hippocampal tissue damage, therefore, shows potential for clinical use.


Assuntos
Antioxidantes/farmacologia , Encéfalo/efeitos dos fármacos , Formaldeído/antagonistas & inibidores , Degeneração Neural/prevenção & controle , Estresse Oxidativo/efeitos dos fármacos , Vitamina E/farmacologia , Animais , Antioxidantes/uso terapêutico , Encéfalo/patologia , Encéfalo/fisiopatologia , Catalase/metabolismo , Formaldeído/toxicidade , Lobo Frontal/efeitos dos fármacos , Lobo Frontal/patologia , Lobo Frontal/fisiopatologia , Hipocampo/efeitos dos fármacos , Hipocampo/patologia , Hipocampo/fisiopatologia , Malondialdeído/metabolismo , Necrose/induzido quimicamente , Necrose/patologia , Necrose/prevenção & controle , Degeneração Neural/induzido quimicamente , Degeneração Neural/patologia , Fármacos Neuroprotetores/farmacologia , Fármacos Neuroprotetores/uso terapêutico , Neurotoxinas/antagonistas & inibidores , Neurotoxinas/toxicidade , Estresse Oxidativo/fisiologia , Ratos , Ratos Wistar , Superóxido Dismutase/metabolismo , Resultado do Tratamento , Vitamina E/uso terapêutico
4.
J Pediatr Endocrinol Metab ; 17(1): 73-6, 2004 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-14960024

RESUMO

We evaluated goiter status and urinary iodine excretion (UIC) of 304 school-children (7-12 years old) 3 years after a law was passed for mandatory production of iodinated salt in an area previously characterized by severe iodine deficiency in Zonguldak, a mountainous city in the West Black Sea region in Turkey. We examined all the children for goiter by palpation, measured sonographic thyroid volumes (STV) and UIC. Eighty-two percent of families had been using iodinated salt. UIC was above 100 microg/l in 71.2% of the children and median UIC was sufficient (143.5 microg/l). The prevalence of goiter was lower at ultrasound (14.6%) than by palpation (19.4%). Median STV values were within recommended normal limits at all ages. Although Zonguldak had been a highly endemic region, it became mildly endemic 3 years after mandatory iodination of salt, with decrease of goiter prevalence.


Assuntos
Bócio/epidemiologia , Bócio/prevenção & controle , Iodo , Iodo/deficiência , Iodo/uso terapêutico , Cloreto de Sódio na Dieta , Criança , Proteção da Criança , Feminino , Humanos , Iodo/urina , Masculino , Prevalência , Glândula Tireoide/anatomia & histologia , Glândula Tireoide/diagnóstico por imagem , Turquia , Ultrassonografia
5.
Clin Chim Acta ; 340(1-2): 153-62, 2004 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-14734207

RESUMO

BACKGROUND: The widespread use of mobile phones (MP) in recent years has raised the research activities in many countries to determine the consequences of exposure to the low-intensity electromagnetic radiation (EMR) of mobile phones. Since several experimental studies suggest a role of reactive oxygen species (ROS) in EMR-induced oxidative damage in tissues, in this study, we investigated the effect of Ginkgo biloba (Gb) on MP-induced oxidative damage in brain tissue of rats. METHODS: Rats (EMR+) were exposed to 900 MHz EMR from MP for 7 days (1 h/day). In the EMR+Gb groups, rats were exposed to EMR and pretreated with Gb. Control and Gb-administrated groups were produced by turning off the mobile phone while the animals were in the same exposure conditions. Subsequently, oxidative stress markers and pathological changes in brain tissue were examined for each groups. RESULTS: Oxidative damage was evident by the: (i) increase in malondialdehyde (MDA) and nitric oxide (NO) levels in brain tissue, (ii) decrease in brain superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and (iii) increase in brain xanthine oxidase (XO) and adenosine deaminase (ADA) activities. These alterations were prevented by Gb treatment. Furthermore, Gb prevented the MP-induced cellular injury in brain tissue histopathologically. CONCLUSION: Reactive oxygen species may play a role in the mechanism that has been proposed to explain the biological side effects of MP, and Gb prevents the MP-induced oxidative stress to preserve antioxidant enzymes activity in brain tissue.


Assuntos
Antioxidantes/farmacologia , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Telefone Celular , Ginkgo biloba , Estresse Oxidativo/efeitos dos fármacos , Extratos Vegetais/farmacologia , Animais , Biomarcadores/análise , Encéfalo/patologia , Campos Eletromagnéticos/efeitos adversos , Feminino , Ratos , Ratos Wistar
6.
J Trop Pediatr ; 48(5): 280-4, 2002 10.
Artigo em Inglês | MEDLINE | ID: mdl-12405170

RESUMO

The aim of this study was to investigate the effects of different doses of iron on haematological status of breastfed infants. One hundred and thirteen infants were randomized into four groups at 5 months of age. Iron supplementation was given at doses of 1 mg/kg/day, 2 mg/kg/day, and 2 mg/kg/every other day in the first three study groups, respectively, and the last group received placebo. The hematological values, except hemoglobin, were higher in the group supplemented with iron at a dose of 2 mg/kg/day, and ferritin values were statistically higher in the group supplemented with iron at a dose of 2 mg/kg/every other day than in the group supplemented with iron at a dose of 1 mg/kg/day. We suggest that intermittent iron supplementation is more effective than a daily regimen in equal dosages.


Assuntos
Anemia Ferropriva/prevenção & controle , Suplementos Nutricionais , Ferro/administração & dosagem , Análise de Variância , Aleitamento Materno , Distribuição de Qui-Quadrado , Feminino , Ferritinas/sangue , Hemoglobinas/análise , Humanos , Lactente , Masculino , Estudos Prospectivos , Resultado do Tratamento
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