Literature DB >> 23559463

Perinatal exposure of patas monkeys to antiretroviral nucleoside reverse-transcriptase inhibitors induces genotoxicity persistent for up to 3 years of age.

Ofelia A Olivero1, Lorangelly Rivera Torres, Sayeh Gorjifard, Dariya Momot, Eryney Marrogi, Rao L Divi, Yongmin Liu, Ruth A Woodward, Marsha J Sowers, Miriam C Poirier.   

Abstract

BACKGROUND: Erythrocebus patas (patas) monkeys were used to model antiretroviral (ARV) drug in human immunodeficiency virus type 1-infected pregnant women.
METHODS: Pregnant patas dams were given human-equivalent doses of ARVs daily during 50% of gestation. Mesenchymal cells, cultured from bone marrow of patas offspring obtained at birth and at 1 and 3 years of age, were examined for genotoxicity, including centrosomal amplification, micronuclei, and micronuclei containing whole chromosomes.
RESULTS: Compared with controls, statistically significant increases (P < .05) in centrosomal amplification, micronuclei, and micronuclei containing whole chromosomes were found in mesenchymal cells from most groups of offspring at the 3 time points.
CONCLUSIONS: Transplacental nucleoside reverse-transcriptase inhibitor exposures induced fetal genotoxicity that was persistent for 3 years.

Entities:  

Keywords:  Erythrocebus patas; abacavir; aneuploidy; centrosomal amplification; lamivudine; mesenchymal fibroblasts; micronuclei; nevirapine; zidovudine

Mesh:

Substances:

Year:  2013        PMID: 23559463      PMCID: PMC3685224          DOI: 10.1093/infdis/jit146

Source DB:  PubMed          Journal:  J Infect Dis        ISSN: 0022-1899            Impact factor:   5.226


  15 in total

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10.  Genotoxic signature in cord blood cells of newborns exposed in utero to a Zidovudine-based antiretroviral combination.

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3.  Mitochondrial compromise in 3-year old patas monkeys exposed in utero to human-equivalent antiretroviral therapies.

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8.  Foetal loss and enhanced fertility observed in mice treated with Zidovudine or Nevirapine.

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9.  Fetal Metabolic Stress Disrupts Immune Homeostasis and Induces Proinflammatory Responses in Human Immunodeficiency Virus Type 1- and Combination Antiretroviral Therapy-Exposed Infants.

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