Jorge Pinto Soares

Prof. Dr. Jorge Pinto Soares

orcid

Research Focus & Metrics

Academic Career Length

17Years (2010-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 June 2014 in Aging
Verified
Journal Article
Open access
JSJorge Pinto Soares
Jorge Pinto Soares
ACAntónio Cortinhas
António Cortinhas
Teresa BentoTeresa Bento
Teresa Bento
JLJosé Carlos Leitão
José Carlos Leitão
ACAndrew Collins
Andrew Collins
MMMaria Paula Mota
Maria Paula Mota
Age‐related DNA damage is regarded as one of the possible explanations of aging. Although a generalized idea about the accumulation of DNA damage with age exists, results found in the literature are inconsistent. To better understand the question of age‐related DNA damage in humans and to identify possible moderator variables, a metaanalysis was conducted. Electronic databases and bibliographies for studies published since 2004 were searched. Summary odds ratios (ORs) and 95% confidence intervals (CIs) for age‐related DNA damage were calculated in a random‐effects model. A total of 76 correlations from 36 studies with 4676 participants were included. Based on our analysis, a correlation between age and DNA damage was found (r=0.230, p=0.000; 95% confidence interval=0.111‐0.342). The test for heterogeneity of variance indicates that the study´s results are significantly high (Q (75)=1754.831, p=0.000). Moderator variables such as smoking habits, technique used, and the tissue/sample analyzed, are shown to influence age‐related DNA damage (p=0.026; p=0.000; p=0.000, respectively). Nevertheless, sex did not show any influence on this relation (p=0.114). In conclusion, this meta‐analysis showed an association between age and DNA damage in humans. It was also found that smoking habits, the technique used, and tissue/sample analyzed, are important moderator variables in age‐related DNA damage.


1 February 2015 in Experimental Gerontology
Verified
Journal Article
Closed access
JSJorge Pinto Soares
Jorge Pinto Soares
ASAmelia Silva
Amelia Silva
SFSandra Fonseca
Sandra Fonseca
MOMaria Manuel Oliveira
Maria Manuel Oliveira
Francisco PeixotoFrancisco Peixoto
Francisco Peixoto
MMMaria Paula Mota
Maria Paula Mota


29 November 2019 in Plants
Verified
Journal Article
Open access
PDF file
ASAmelia Silva
Amelia Silva
SSSandra C. Silva
Sandra C. Silva
JSJorge Pinto Soares
Jorge Pinto Soares
CMCarlos Martins-Gomes
Carlos Martins-Gomes
João Paulo TeixeiraJoão Paulo Teixeira
João Paulo Teixeira
Isabel GaivãoIsabel Gaivão
Isabel Gaivão
Ginkgo biloba L. leaf extracts and herbal infusions are used worldwide due to the health benefits that are attributed to its use, including anti-neoplastic, anti-aging, neuro-protection, antioxidant and others. The aim of this study was to evaluate the effect of an aqueous Ginkgo biloba extract on HepG2 cell viability, genotoxicity and DNA protection against paraquat-induced oxidative damage. Exposure to paraquat (PQ), over 24 h incubation at 1.0 and 1.5 µM, did not significantly reduce cell viability but induced concentration and time-dependent oxidative DNA damage. Ginkgo biloba leaf extract produced dose-dependent cytotoxicity (IC50 = 540.8 ± 40.5 µg/mL at 24 h exposure), and short incubations (1 h) produced basal and oxidative DNA damage (>750 and 1500 µg/mL, respectively). However, lower concentrations (e.g., 75 µg/mL) of Ginkgo biloba leaf extract were not cytotoxic and reduced basal DNA damage, indicating a protective effect at incubations up to 4 h. On the other hand, longer incubations (24 h) induced oxidative DNA damage. Co-incubation of HepG2 cells for 4 h, with G. biloba leaf extract (75 µg/mL) and PQ (1.0 or 1.5 µM) significantly reduced PQ-induced oxidative DNA damage. In conclusion, the consumption of Ginkgo biloba leaf extract for long periods at high doses/concentrations is potentially toxic; however, low doses protect the cells against basal oxidative damage and against environmentally derived toxicants that induce oxidative DNA damage.

21 March 2018 in International Journal of Sports Medicine
Verified
Journal Article
Closed access
PDF file
AFAna Cristina Corrêa Figueira
Ana Cristina Corrêa Figueira
ACAntónio Cortinhas
António Cortinhas
JSJorge Pinto Soares
Jorge Pinto Soares
JLJosé Carlos Leitão
José Carlos Leitão
RFRita Pinho Ferreira
Rita Pinho Ferreira
JDJosé Alberto Duarte
José Alberto Duarte
The use of preclinical models to investigate antitumor effects of exercise on breast tumor (BT) development and progression are critical. However, published results have not been quantitatively summarized or examined for potential exercise-moderating variables. We conducted this review to summarize and quantify the effect-size of exercise on BT outcomes in preclinical studies. A literature search was performed in MEDLINE, PubMed, Web of Science and System for Information on Grey Literature in Europe (SIGLE) databases. Risk of bias was assessed using SYRCLE’s RoB tool. A total of 116 correlations were performed to analyze 28 preclinical studies published through December 2016, which included 2,085 animals and 51 exercise programs. Positive effects of small, medium and large magnitude were observed in tumor incidence, growth and multiplicity, respectively. In the tumor microenvironment, positive effects of large magnitude were also observed in proliferation and apoptosis but not in angiogenesis. Moderator variables correlated with higher intervention effects were identified along with a considerable heterogeneity in exercise protocols that precluded us from clearly perceiving the benefits of exercise exposure. In conclusion, exercise performed under specific conditions benefits BT outcomes. Preclinical studies with exercise designs mimicking exercise exposure that can be used in clinical contexts are needed.