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1.
Int J Mol Sci ; 25(16)2024 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-39201580

RESUMO

Congenital heart disease (CHD) can be complicated by pulmonary arterial hypertension (PAH). Cardiopulmonary bypass (CPB) for corrective surgery may cause endothelial dysfunction, involving endothelin-1 (ET-1), circulating endothelial cells (CECs), and endothelial progenitor cells (EPCs). These markers can gauge disease severity, but their levels in children's peripheral blood still lack consensus for prognostic value. The aim of our study was to investigate changes in ET-1, cytokines, and the absolute numbers (Ɲ) of CECs and EPCs in children 24 h before and 48 h after CPB surgery to identify high-risk patients of complications. A cohort of 56 children was included: 41 cases with CHD-PAH (22 with high pulmonary flow and 19 with low pulmonary flow) and 15 control cases. We observed that Ɲ-CECs increased in both CHD groups and that Ɲ-EPCs decreased in the immediate post-surgical period, and there was a strong negative correlation between ET-1 and CEC before surgery, along with significant changes in ET-1, IL8, IL6, and CEC levels. Our findings support the understanding of endothelial cell precursors' role in endogenous repair and contribute to knowledge about endothelial dysfunction in CHD.


Assuntos
Ponte Cardiopulmonar , Citocinas , Células Endoteliais , Células Progenitoras Endoteliais , Endotelina-1 , Cardiopatias Congênitas , Humanos , Endotelina-1/sangue , Endotelina-1/metabolismo , Células Progenitoras Endoteliais/metabolismo , Cardiopatias Congênitas/cirurgia , Cardiopatias Congênitas/sangue , Cardiopatias Congênitas/metabolismo , Cardiopatias Congênitas/patologia , Masculino , Feminino , Ponte Cardiopulmonar/efeitos adversos , Células Endoteliais/metabolismo , Citocinas/sangue , Citocinas/metabolismo , Criança , Pré-Escolar , Lactente , Biomarcadores/sangue , Estudos de Casos e Controles
2.
Mutagenesis ; 28(2): 219-25, 2013 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-23408844

RESUMO

Patients with chronic kidney disease (CKD) have signs of genomic instability and, as a consequence, extensive genetic damage, possibly due to accumulation of uraemic toxins, oxidative stress mediators and other endogenous substances with genotoxic properties. We explored factors associated with the presence and background levels of genetic damage in CKD. A cross-sectional study was performed in 91 CKD patients including pre-dialysis (CKD patients; n = 23) and patients undergoing peritoneal dialysis (PD; n = 33) or haemodialysis (HD; n = 35) and with 61 healthy subjects, divided into two subgroups with the older group being in the age range of the patients, serving as controls. Alkaline comet assay and cytokinesis-block micronucleus assay in peripheral blood lymphocytes were used to determine DNA and chromosome damage, respectively, present in CKD. Markers of oxidative stress [malondialdehyde (MDA), advanced glycation end products (AGEs), thiols, advanced oxidation protein products and 8-hydroxy-2'-deoxyguanosine] and markers of inflammation (C-reactive protein, interleukin-6 and tumour necrosis factor alpha) were also measured. Micronucleus (MN) frequency was significantly higher (P < 0.05) in the CKD group (46±4‰) when compared with the older control (oC) group (27.7±14). A significant increase in MN frequency (P < 0.05) was also seen in PD patients (41.9±14‰) versus the oC group. There was no statistically significant difference for the HD group (29.7±15.6‰; P = NS) versus the oC group. Comet assay data showed a significant increase (P < 0.001) of tail DNA intensity in cells of patients with CKD (15.6±7%) with respect to the total control (TC) group (11±1%). PD patients (14.8±7%) also have a significant increase (P < 0.001) versus the TC group. Again, there was no statistically significant difference for the HD group (12.5±3%) compared with the TC group. Patients with MN values in the upper quartile had increased cholesterol, triglycerides, AGEs and MDA levels and lower albumin levels. Multiple logistic regression analysis showed that male gender, diabetes and treatment modality were independently associated with higher levels of DNA damage. Our results suggest that oxidative stress, diabetes, gender and dialysis modality in CKD patients increased DNA and chromosome damage. To confirm these data, prospective clinical trials need to be performed.


Assuntos
Instabilidade Cromossômica , Diálise Peritoneal/efeitos adversos , Diálise Renal/efeitos adversos , Insuficiência Renal Crônica/fisiopatologia , 8-Hidroxi-2'-Desoxiguanosina , Adulto , Idoso , Biomarcadores/sangue , Proteína C-Reativa/análise , Proteína C-Reativa/metabolismo , Ensaio Cometa , Estudos Transversais , Dano ao DNA , Desoxiguanosina/análogos & derivados , Desoxiguanosina/sangue , Feminino , Produtos Finais de Glicação Avançada/sangue , Humanos , Inflamação , Interleucina-6/sangue , Modelos Logísticos , Linfócitos/patologia , Masculino , Malondialdeído/sangue , Testes para Micronúcleos , Pessoa de Meia-Idade , Estresse Oxidativo , Insuficiência Renal Crônica/genética , Albumina Sérica/análise , Triglicerídeos/sangue , Fator de Necrose Tumoral alfa/sangue
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