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James J. Salazar

Researcher at Galveston College

Publications -  7
Citations -  245

James J. Salazar is an academic researcher from Galveston College. The author has contributed to research in topics: DNA damage & DNA repair. The author has an hindex of 5, co-authored 7 publications receiving 238 citations. Previous affiliations of James J. Salazar include University of Texas Medical Branch.

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Preferential mitochondrial DNA injury caused by glucose oxidase as a steady generator of hydrogen peroxide in human fibroblasts

TL;DR: Data show that GO-generated H202 causes acute damage to mtDNA and function, and demonstrate that this organelle is an important site for the cellular toxicity of ROS.
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Persistence, gestation stage-dependent formation and interrelationship of benzo[a]pyrene-induced DNA adducts in mothers, placentae and fetuses of Erythrocebus patas monkeys.

TL;DR: The results suggest that placental adduction accurately indicates fetal exposure and maximal sensitivity to transplacental DNA damage may be during mid-gestation, which is critical determinants in overall fetal risk to genetic damage.
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A model of sensitivity: 1,3-butadiene increases mutant frequencies and genomic damage in mice lacking a functional microsomal epoxide hydrolase gene.

TL;DR: The lack of mEH activity increases the genetic sensitivity of mice exposed to BD and BDO2, and a mechanistic understanding of the observed variation in human genetic sensitivity following exposure to BD is facilitated.
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Genetic Evidence for XPC-KRAS Interactions During Lung Cancer Development.

TL;DR: It is demonstrated that induced expression of oncogenic KRAS(G12V) led to increased levels of reactive oxygen species (ROS) as well as DNA damage, and both can be suppressed by anti-oxidants, suggesting that XPC may help repair DNA damage caused by KRAS-mediated production of ROS.
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Absence of formation of benzo[a]pyrene/DNA adducts in the cuttlefish (Sepia officinalis, Mollusca: Cephalopoda).

TL;DR: The dose of the carcinogen injected into the cuttlefish was 2—4 times higher than the dose resulting in the formation of a high level of B[a]P/DNA adducts in the vertebrates, which could explain the absence from the literature of reports of tumors in cephalopods.