Increase in DNA polymerase gamma in the hearts of adriamycin-administered rats.

Abstract:

It is hypothesized that the cause of myocardiopathy is oxidative damage to mitochondrial DNA. To clarify this hypothesis, DNA polymerase gamma activity, which is related to the final step of mitochondrial DNA repair or renewal, was measured. One cycle of treatment consisted of five injections of adriamycin over 5 days at a dose of 1 mg/kg of body weight per day and then 2 days resting time. DNA polymerase gamma activities in the heart after one cycle of treatment were lower than the control level. However, DNA polymerase gamma activities increased with continued adriamycin treatment, reaching a maximum level in the heart at 14 days after two cycles of adriamycin treatment. Induction of DNA polymerase gamma activity was found in rat heart following three and four cycles of administration. Under these conditions, it is doubtful that mitochondrial DNA is the direct target of adriamycin administration. The damaged mitochondrial DNA may be protected by actions of the renewal or repair systems, maintaining mitochondrial function in the heart. Rat hearts at 7 days after one cycle of adriamycin treatment show morphological changes in the mitochondria that include matrix swelling and cristae disorganization, as seen in cardiac cells by electron microscopy; however, 28 days after treatment, the mitochondria appear to have recovered.

Polymerases:

Topics:

Status:

new topics/pols set partial results complete validated

Results:

No results available for this paper.

Entry validated by:

Log in to edit reference All References

Using Polbase tables:

Sorting:

Tables may be sorted by clicking on any of the column titles. A second click reverses the sort order. <Ctrl> + click on the column titles to sort by more than one column (e.g. family then name).

Filtering:

It is also possible to filter the table by typing into the search box above the table. This will instantly hide lines from the table that do not contain your search text.