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1.
Hum Exp Toxicol ; 36(10): 1071-1080, 2017 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-27895098

RESUMO

Mineral trioxide aggregate (MTA) is a calcium silicate dental cement used for various applications in dentistry. This study was undertaken to test whether the presence of three commercial brands of calcium silicate dental cements in the dental extraction socket of rats would affect the brain aluminium (Al) levels and oxidative stress parameters. Right upper incisor was extracted and polyethylene tubes filled with MTA Angelus, MTA Fillapex or Theracal LC, or left empty for the control group, were inserted into the extraction socket. Rats were killed 7, 30 or 60 days after operation. Brain tissues were obtained before killing. Al levels were measured by atomic absorption spectrometry. Thiobarbituric acid reactive substances (TBARS) levels, catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities were determined using spectrophotometry. A transient peak was observed in brain Al level of MTA Angelus group on day 7, while MTA Fillapex and Theracal LC groups reached highest brain Al level on day 60. Brain TBARS level, CAT, SOD and GPx activities transiently increased on day 7 and then returned to almost normal levels. This in vivo study for the first time indicated that initial washout may have occurred in MTA Angelus, while element leaching after the setting is complete may have taken place for MTA Fillapex and Theracal LC. Moreover, oxidative stress was induced and antioxidant enzymes were transiently upregulated. Further studies to search for oxidative neuronal damage should be done to completely understand the possible toxic effects of calcium silicate cements on the brain.


Assuntos
Compostos de Alumínio/toxicidade , Alumínio/metabolismo , Encéfalo/efeitos dos fármacos , Compostos de Cálcio/toxicidade , Cimentos Dentários/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Óxidos/toxicidade , Silicatos/toxicidade , Animais , Encéfalo/metabolismo , Catalase/metabolismo , Combinação de Medicamentos , Glutationa Peroxidase/metabolismo , Masculino , Ratos Wistar , Superóxido Dismutase/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo , Alvéolo Dental
2.
Hum Exp Toxicol ; 32(5): 483-91, 2013 May.
Artigo em Inglês | MEDLINE | ID: mdl-23111888

RESUMO

This study aimed to determine whether the coding (A4889G) and noncoding region (T6235C) polymorphisms of the gene coding for cytochrome P4501A1 (CYP1A1), a xenobiotic-metabolizing enzyme responsible for the metabolism of carcinogenic polycyclic aromatic hydrocarbons, are involved in the pathogenesis of ischemic stroke in Turkish population. Study group consisted of 226 ischemic stroke patients and 113 controls. Genotypes were attained by allele-specific polymerase chain reaction (PCR) for A4889G and PCR/restriction fragment length polymorphism analysis for T6235C. Frequency of 6235C allele was significantly lower in patients (0.151) compared with controls (0.226, P = 0.015). Prevalence of hypertension and hypertension-associated ischemic stroke risk was lower for 6235C allele carriers. This allele decreased ischemic stroke risk twofold (adjusted odds ratio = 0.48, P = 0.005). There was almost no difference in 4889G allele frequencies in patients (0.445) and controls (0.425). However, prevalence of hypertension was lower in 4889G allele carriers when compared with the wild-type genotypes. In addition, risk of ischemic stroke for smoker and hypertensive individuals was lower when they have at least one 4889G allele. The present study demonstrated that CYP1A1 genetic variants contribute to interindividual variability in smoking- and hypertension-induced ischemic stroke risk.


Assuntos
Isquemia Encefálica/genética , Citocromo P-450 CYP1A1/genética , Hipertensão/complicações , Fumar/efeitos adversos , Acidente Vascular Cerebral/genética , Adulto , Idoso , Isquemia Encefálica/etiologia , HDL-Colesterol/sangue , LDL-Colesterol/sangue , Feminino , Genótipo , Humanos , Hipertensão/sangue , Masculino , Pessoa de Meia-Idade , Risco , Acidente Vascular Cerebral/etiologia
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