Author
Listed:
- Thiago Aley Brites de Freitas
(Medical Genetics Service, Hospital de Clínicas de Porto Alegre, Porto Alegre, RS 90035-903, Brazil)
- Roberta Passos Palazzo
(Medical Genetics Service, Hospital de Clínicas de Porto Alegre, Porto Alegre, RS 90035-903, Brazil)
- Fabiana Michelsen De Andrade
(Health Science Institute, Feevale University, RS 239, Novo Hamburgo, RS 93352-000, Brazil)
- César Luis Reichert
(Health Science Institute, Feevale University, RS 239, Novo Hamburgo, RS 93352-000, Brazil)
- Flávio Pechansky
(Center for Drug and Alcohol Research, Hospital de Clínicas de Porto Alegre and Universidade Federal do Rio Grande do Sul, Porto Alegre, RS 90035-903, Brazil)
- Félix Kessler
(Center for Drug and Alcohol Research, Hospital de Clínicas de Porto Alegre and Universidade Federal do Rio Grande do Sul, Porto Alegre, RS 90035-903, Brazil)
- Caroline Brunetto De Farias
(Laboratório de Pesquisas em Câncer, Hospital de Clínicas de Porto Alegre, Porto Alegre, RS 90035-903, Brazil)
- Gisele Gomes De Andrade
(Medical Genetics Service, Hospital de Clínicas de Porto Alegre, Porto Alegre, RS 90035-903, Brazil)
- Sandra Leistner-Segal
(Medical Genetics Service, Hospital de Clínicas de Porto Alegre, Porto Alegre, RS 90035-903, Brazil)
- Sharbel Weidner Maluf
(Medical Genetics Service, Hospital de Clínicas de Porto Alegre, Porto Alegre, RS 90035-903, Brazil)
Abstract
Recent research suggests that crack cocaine use alters systemic biochemical markers, like oxidative damage and inflammation markers, but very few studies have assessed the potential effects of crack cocaine at the cellular level. We assessed genome instability by means of the comet assay and the cytokinesis-block micronucleus technique in crack cocaine users at the time of admission to a rehabilitation clinic and at two times after the beginning of withdrawal. Thirty one active users of crack cocaine and forty control subjects were evaluated. Comparison between controls and crack cocaine users at the first analysis showed significant differences in the rates of DNA damage ( p = 0.037). The frequency of micronuclei (MN) ( p < 0.001) and nuclear buds (NBUDs) ( p < 0.001) was increased, but not the frequency of nucleoplasmic bridges (NPBs) ( p = 0.089). DNA damage decreased only after the end of treatment ( p < 0.001). Micronuclei frequency did not decrease after treatment, and nuclear buds increased substantially. The results of this study reveal the genotoxic and mutagenic effects of crack cocaine use in human lymphocytes and pave the way for further research on cellular responses and the possible consequences of DNA damage, such as induction of irreversible neurological disease and cancer.
Suggested Citation
Thiago Aley Brites de Freitas & Roberta Passos Palazzo & Fabiana Michelsen De Andrade & César Luis Reichert & Flávio Pechansky & Félix Kessler & Caroline Brunetto De Farias & Gisele Gomes De Andrade &, 2014.
"Genomic Instability in Human Lymphocytes from Male Users of Crack Cocaine,"
IJERPH, MDPI, vol. 11(10), pages 1-13, September.
Handle:
RePEc:gam:jijerp:v:11:y:2014:i:10:p:10003-10015:d:40673
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