3 research outputs found
Chronic ethanol consumption in mice does not induce DNA damage in somatic or germ cells, evaluated by the bone marrow micronucleous assay and the dominant lethal mutation assay
IndexaciĂłn: Web of Science; ScieloAlthough alcohol is known to be a carcinogen for humans, ethanol-genotoxicity studies are incomplete. Ethanol seems not to be a bacterial mutagen, but the results are conflicting in rodent assays. We investigate the genotoxicity in the bone marrow micronucleus (MN) test and in the dominant lethal mutation (DLM) assay using two long-term ethanol exposure protocols. In the MN test, mice consumed three doses (5, 10 and 15% v/v) for 32 weeks. MN induction was compared to two control groups of 5- and 38-week-old mice (the ages of the treated mice when the treatment was initiated and when they were killed, respectively). For the three groups treated with ethanol there was no significant increase in MN induction as compared to the first control group, but observed MN frequencies were significantly lower than in the 38-week-old control group. This suggests a protective effect against genotoxic damage caused by aging, probably due to ethanol action as a hydroxyl radical scavenger.
In the DLM assay, male mice drank ethanol at 15% or 30% (v/v) for 20 weeks. In both groups the number of dead implants was similar to the control, but there was a significant reduction in total implants, indicating a pre-implantation loss.http://ref.scielo.org/7b9mt
Chronic ethanol consumption in mice does not induce DNA damage in somatic or germ cells, evaluated by the bone marrow micronucleous assay and the dominant lethal mutation assay
Although alcohol is known to be a carcinogen for humans, ethanol-genotoxicity studies are incomplete. Ethanol seems not to be a bacterial mutagen, but the results are conflicting in rodent assays. We investigate the genotoxicity in the bone marrow micronucleus (MN) test and in the dominant lethal mutation (DLM) assay using two long-term ethanol exposure protocols. In the MN test, mice consumed three doses (5, 10 and 15% v/v) for 32 weeks. MN induction was compared to two control groups of 5- and 38-week-old mice (the ages of the treated mice when the treatment was initiated and when they were killed, respectively). For the three groups treated with ethanol there was no significant increase in MN induction as compared to the first control group, but observed MN frequencies were significantly lower than in the 38-week-old control group. This suggests a protective effect against genotoxic damage caused by aging, probably due to ethanol action as a hydroxyl radical scavenger. In the DLM assay, male mice drank ethanol at 15% or 30% (v/v) for 20 weeks. In both groups the number of dead implants was similar to the control, but there was a significant reduction in total implants, indicating a pre-implantation loss
Preliminary evaluation of DNA damage related with the smoking habit measured by the comet assay in whole blood cells
ArtĂculo de publicaciĂłn ISIThe alkaline single-cell gel electrophoresis (SCGE)
assay, also called the comet assay, is a rapid and
simple method for the detection of DNA damage in
individual cells. The objective of this study was to
establish if the alkaline SCGE assay in whole blood
cells gives similar results as the same method in
isolated lymphocytes, because whole blood cells are
simpler and more economical to use, specifically in
human genotoxic biomonitoring. To validate the
method, we first used mouse blood cells, because
mouse is one of the most commonly used animals in
genetic toxicology testing. Groups of seven CF1 male
mice were given i.p. injections of relatively low doses
of methyl methanesulfonate (25 mg/kg body weight), a
direct acting genotoxic agent, or cyclophosphamide
(50 mg/kg body weight), which requires metabolic
activation. Three, 6, 8, 12, 16, 20, and 65 hours after
treatment, 5 ML of blood were collected from each
animal and were processed for the alkaline SCGE
assay. On the basis of an analysis of tail moment, the
results showed that this assay can detect DNA damage
induced by both kinds of alkylating mutagens. We
then did a preliminary study to assess the status of
DNA damage in a young (19 to 23 years old) healthy
population of male smokers (n = 6) and nonsmokers
(n = 6) using the comet assay in whole blood cells.
A significant difference was observed between the
two groups, showing that the method is able to detect
DNA damage in the smoking group despite
the short time that the volunteers had actually been
smoking