Journal Issue:
Dose-Response: An International Journal: Volume 11, Issue 1

No Thumbnail Available
Volume
Number
Issue Date
2013-31-03
Journal Title
Journal ISSN
Articles
Publication
Dose-Response Vol 11, no 1, Cover
(2013-03-01)
Publication
Publication
SHORT-TERM PCB (AROCLOR 1254) TOXICITY ON FEW PHOSPHATASES IN MICE BRAIN
(2013-03-01) Pathak, Shweta; Kundu, Rahul
The present communication reports the dose and duration dependent toxicity of a PCB, Aroclor 1254, to a few ion dependent ATPases, Acid phosphatase, Alkaline phosphatase and Glucose-6-phosphatase in the whole brain tissue of mice. Two groups of mice were subjected to two sublethal doses (0.1 and 1 mg kgbw-1 day-1) of PCB orally and exposed for 4, 8 or12 days. A separate control group received the corn oil vehicle for the same exposure times. The observed results indicated exposure duration dependent changes in the enzymatic levels in the brain. The results suggest that the alteration in the enzymatic activity was possibly due to imposed oxidative stress generated by Aroclor 1254 on membrane-bound ion-dependent ATPases and other phosphatases in the brain tissue.
Publication
FIRST GENERATION STOCHASTIC GENE EPISILENCING (STEP1) MODEL AND APPLICATIONS TO IN VITRO CARCINOGEN EXPOSURE
(2013-03-01) Scott, Bobby R
A novel first-generation stochastic gene episilencing (STEP1) model is introduced for quantitatively characterizing the probability of in vitro epigenetically silencing (episilencing) specific tumor-suppressor-microRNA (miRNA) genes by carcinogen exposure. Although the focus is mainly on in-vitro exposure of human cells to ionizing radiation, the mathematical formulations presented are general and can be applied to other carcinogens. With the STEP1 model, a fraction fj of the surviving target cells can have their tumorsuppressor- miRNA gene of type j silenced while the remaining fraction, 1 – fj, of the surviving cells do not undergo gene episilencing. Suppressor gene episilencing is assumed to arise as a Poisson process characterized with and exponential distribution of episilencing doses with mean dj. In addition to providing mathematical functions for evaluating the single- target-gene episilencing probability, functions are also provided for the multi-target-gene episilencing probability for simultaneously silencing of multiple tumor-suppressor-miRNA genes. Functional relationships are first developed for moderate doses where adaptive responses are unlikely and are then modified for low doses where adaptation can occur. Results apply to a specific follow-up time t after carcinogen exposure that exceeds the maximum time for the occurrence of an induced episilencing event.
Description
Keywords