Academic Thesis

Basic information

Name Katayama Keiichi
Belonging department
Occupation name
researchmap researcher code B000305947
researchmap agency Okayama University of Science

Title

5-azacytidine induced apoptosis in lymphoid and hematopoietic organs of adult mice

Bibliography Type

 

Author

Md. Mokbul Hossain
Hiroyuki Nakayama
Junko Shinozuka
Kei-Ichi Katayama
Kazuhiko Suzuki
Kunio Doi

Summary

The present study deals with the effects of 5-azacytidine (5AzC) on the lymphoid and hematopoietic tissues in adult mice. Seven-week-old, male BALB/c mice were injected with 5AzC (100mg/kg) intraperitoneally, and the thymus, spleen, and bone marrow were examined for cellular proliferative activity and apoptotic changes. In 5AzC-treated mice, the number of proliferative cell nuclear antigen (PCNA)-positive cells began to decrease at 6 hours after treatment (AT) in the thymic cortex and bone marrow, and at 12 hours AT in the splenic white pulp. The number of TUNEL-positive cells strikingly increased up to 24 hours AT in the thymic cortex, to 12 hours AT in the splenic white pulp, and to 6 hours AT in the bone marrow, and decreased thereafter in all tissues. The number of immature myeloid and erythroid cells in the bone marrow decreased after 5AzC-treatment. Electron microscopic study revealed nuclear condensation and fragmentation in pyknotic or karyorrhectic thymic lymphocytes. DNA electrophoresis of the thymus and bone marrow from 5AzC-treated mice at 12 hours AT showed a typical ladder formation. These findings indicate the apoptotic effect of 5AzC on dividing lymphoid and hematopoietic cells even in adult mice.

Magazine(name)

Journal of Toxicologic Pathology

Publisher

Japanese Society of Toxicologic Pathology

Volume

13

Number Of Pages

4

StartingPage

231

EndingPage

236

Date of Issue

2000

Referee

Exist

Invited

Not exist

Language

English

Thesis Type

Research papers (academic journals)

ISSN

 

DOI

10.1293/tox.13.231

NAID

 

PMID

 

J-GLOBAL ID

 

arXiv ID

 

ORCID Put Code

 

DBLP ID