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1.
Biol Trace Elem Res ; 153(1-3): 237-42, 2013 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-23591959

RESUMO

This study aims to explore the effect of selenium in fluoride-induced renal cell apoptosis in rats and determine the optimal level of selenium in drinking water to prevent fluorosis. Experimental animals were divided into a control group, a sodium fluoride-treated group (NaF, 50 mg/L), three sodium selenite-treated groups (Na2SeO3, 0.375, 0.75, and 1.5 mg/L), and three selenium + NaF-treated groups (Na2SeO3, 0.375, 0.75, and 1.5 mg/L; NaF, 50 mg/L). Ultrastructural changes in the kidney tissues of each group were observed by transmission electron microscopy. Apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay and the expressions of Bcl-2 and Bax proteins were detected by immunohistochemical methods. The expressions of Bcl-2 and Bax mRNA were detected by reverse transcription-polymerase chain reaction. The results showed that Bcl-2, Bax, and Bax/Bcl-2 protein expressions in the fluoride and high selenium groups were highly elevated compared with the control group (P < 0.01). Bax expression in the low selenium group and Bcl-2, Bax, and Bax/Bcl-2 protein expressions in the moderate selenium groups were observably elevated (P < 0.05). Bax and Bax/Bcl-2 expressions in the fluoride group and Bax mRNA expression in the high selenium group were highly elevated (P < 0.01). Bax/Bcl-2 mRNA expression in the high selenium group was also highly elevated (P < 0.05). Compared with the fluoride group, the group treated with low selenium has Bax protein expression that was observably reduced (P < 0.05); the group treated with moderate selenium has Bcl-2 protein expression that was observably elevated (P < 0.05), Bax protein expression that was highly reduced (P < 0.01), and Bax/Bcl-2 protein expression that was observably reduced (P < 0.05); the group treated with high selenium has Bcl-2 protein expression that was highly elevated (P < 0.01), Bax protein expression that was highly elevated (P < 0.01), and Bax/Bcl-2 protein expression that was highly reduced (P < 0.01); the groups treated with moderate selenium and high selenium have Bax mRNA expression that was highly reduced (P < 0.01), and the groups treated with high selenium have Bax/Bcl-2 mRNA expression that was observably reduced (P < 0.05). Selenium may inhibit the apoptosis of renal cells in fluorosis rats by regulating the expressions of Bcl-2 and Bax. The optimal dose of Na2SeO3 to protect against fluoride-induced renal cell apoptosis was determined to be 1.5 mg/L.


Assuntos
Apoptose/efeitos dos fármacos , Fluorose Dentária/patologia , Rim/efeitos dos fármacos , Selênio/farmacologia , Animais , Sequência de Bases , Primers do DNA , Rim/metabolismo , Rim/patologia , Masculino , Reação em Cadeia da Polimerase , RNA Mensageiro/genética , Ratos , Ratos Sprague-Dawley , Proteína X Associada a bcl-2/genética , Proteína X Associada a bcl-2/metabolismo
2.
Exp Toxicol Pathol ; 64(6): 565-8, 2012 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-21146966

RESUMO

This study is to explore the effect of selenium and fluoride on blood antioxidant capacity of rats, and try to find out the optimal level of selenium in drinking water against fluorosis. Animals were divided into control group, sodium fluoride treated group (NaF, 50 mg/L) and selenium+NaF treated group (sodium selenite 0.375, 0.75, 1.5 mg/L) in water were respectively administered to male rats, which were decapitated after 6 months. Their blood was collected for GSH-Px activity, plasma SOD activity, T-AOC assay, uric acid assay, sialic acid (SA) content and MDA content, and the fluidity of erythrocyte membrane by electron spin resonance (ESR) was analyzed. The results showed that, compared with the control group, the blood antioxidant capacity of the rats exposed to fluoride was down-regulated significantly (P<0.05, P<0.01), MDA content increased significantly (P<0.05), the fluidity of erythrocyte membrane decreased (P<0.05, P<0.01). Meanwhile, the treatments of selenium along with NaF compared with fluorosis group, SOD activity, GSH-Px activity and T-AOC assay increased respectively, MDA content decreased significantly (P<0.05) in NaF+Se (Se 0.75, 1.5 mg/L) treated groups, uric acid level was up-regulated, but had no statistical significant difference (P>0.05). The fluidity of erythrocyte membrane showed significant increase (P<0.05), the content of SA was lower. Fluorosis could induce the decline of blood antioxidant capacity and the fluidity of erythrocyte membrane, as evident in this study, and Se at different levels possess some antagonistic effects on blood induced by fluoride. However, high dose of selenium (1.5 mg/L) is the optimum concentration.


Assuntos
Antioxidantes/farmacologia , Cariostáticos/toxicidade , Eritrócitos/efeitos dos fármacos , Fluoretos/toxicidade , Fluidez de Membrana/efeitos dos fármacos , Selênio/farmacologia , Animais , Membrana Celular/efeitos dos fármacos , Espectroscopia de Ressonância de Spin Eletrônica , Fluorose Dentária/sangue , Fluorose Dentária/prevenção & controle , Masculino , Ratos , Ratos Sprague-Dawley
3.
Exp Toxicol Pathol ; 63(5): 407-11, 2011 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-20304620

RESUMO

The study investigated the neurotoxicity of drinking water fluorosis in rat hippocampus. Just weaning male Sprague-Dawley (SD) rats were given 15, 30, 60 mg/L NaF solution and tap water for 9 months. The calcium ion concentration ([Ca(2+)]) in synaptosomes was measured by double wavelength fluorescence spectrophotometer and the expression level of nuclear transcription factor kappa-B ρ65 (NF-κB ρ65) in hippocampal CA3 region was measured by immunohistochemistry. The results showed that [Ca(2+)] significantly increased (F = 33.218, P < 0.01) in moderate fluoride group compared with the control group, and the expression level of NF-κB ρ65 in CA3 region presented an increasing trend as fluoride concentration increased. These results indicate that increase of synaptosomes [Ca(2+)] and NF-κB ρ65 expression level may be the molecular basis of central nervous system damage caused by chronic fluoride intoxication. NF-κB ρ65 in CA3 region is probably a target molecule for fluorosis.


Assuntos
Região CA3 Hipocampal/metabolismo , Cálcio/metabolismo , Síndromes Neurotóxicas/metabolismo , Fluoreto de Sódio/toxicidade , Fator de Transcrição RelA/metabolismo , Animais , Região CA3 Hipocampal/patologia , Relação Dose-Resposta a Droga , Intoxicação por Flúor/etiologia , Intoxicação por Flúor/metabolismo , Intoxicação por Flúor/patologia , Fluorose Dentária/etiologia , Fluorose Dentária/metabolismo , Fluorose Dentária/patologia , Masculino , Síndromes Neurotóxicas/etiologia , Síndromes Neurotóxicas/patologia , Ratos , Ratos Sprague-Dawley , Sinaptossomos/metabolismo , Sinaptossomos/patologia , Desmame
4.
Yao Xue Xue Bao ; 37(1): 1-4, 2002 Jan.
Artigo em Chinês | MEDLINE | ID: mdl-12579889

RESUMO

AIM: To study the effects of puerarin on learning-memory behavior of aging mice induced by D-galactose and its possible mechanism of action. METHODS: The aging mice were induced by s.c. 0.12 g.kg-1 D-galactose for 6 weeks. The aging mice were treated with three doses of puerarin once a day for 5 weeks. The spontaneous behavior and the learning memory behavior were tested in the aging mice using open field and Y-maze at the next day after the last treatment. The structure of Gray I synaptic interface in the CA3 area of the hippocampus was quantitatively analyzed by electronic microscope and computer image processing appliance. RESULTS: Compared with the D-galactose control group, puerarin (60 mg.kg-1) was shown to increase significantly the spontaneous behavior and explorative response in the open field, and improve remarkablely the learning and memory ability of the aging mice induced by D-galactose. Meanwhile, the thickness of post-synaptic density (PSD) was increased, and the width of the synaptic cleft in the hippocampus CA3 area was shortened. CONCLUSION: Puerarin showed an improvement effect against the memory impairment in the modelling aging-mice induced by D-galactose. A pathological alteration of synaptic interface structure in hippocampus of the mice may be involved in the effect.


Assuntos
Envelhecimento/efeitos dos fármacos , Galactose/farmacologia , Hipocampo/efeitos dos fármacos , Isoflavonas/farmacologia , Memória/efeitos dos fármacos , Sinapses/efeitos dos fármacos , Animais , Comportamento Animal/efeitos dos fármacos , Feminino , Hipocampo/patologia , Masculino , Aprendizagem em Labirinto/efeitos dos fármacos , Camundongos , Fármacos Neuroprotetores/farmacologia , Distribuição Aleatória , Sinapses/patologia
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