Talk to the Veterans Crisis Line now
U.S. flag
An official website of the United States government

Health Services Research & Development

Go to the ORD website
Go to the QUERI website

HSR&D Citation Abstract

Search | Search by Center | Search by Source | Keywords in Title

Ethambutol induces PKC-dependent cytotoxic and antiproliferative effects on human retinal pigment cells.

Tsai RK, Chang CH, Hseu CM, Chang SM, Wu JR, Wang HZ, Wu WS. Ethambutol induces PKC-dependent cytotoxic and antiproliferative effects on human retinal pigment cells. Experimental Eye Research. 2008 Dec 1; 87(6):594-603.

Dimensions for VA is a web-based tool available to VA staff that enables detailed searches of published research and research projects.

If you have VA-Intranet access, click here for more information vaww.hsrd.research.va.gov/dimensions/

VA staff not currently on the VA network can access Dimensions by registering for an account using their VA email address.
   Search Dimensions for VA for this citation
* Don't have VA-internal network access or a VA email address? Try searching the free-to-the-public version of Dimensions



Abstract:

Ethambutol (EMB)-induced ocular side effects may involve the influence on functions of retinal pigment epithelium (RPE), in addition to EMB-induced optic neuropathy. To address this issue, the molecular and cellular effects of EMB on RPE including growth regulation, morphological responses, phagocytic activity, and the relevant signaling pathways were investigated. EMB (at optimal concentration 8.0mM) can trigger cell cycle arrest in both RPE50 and ARPE19 cells, accompanied by reduced DNA synthesis. EMB also induced cytoplasmic vacuole formation in both RPE cell lines. Under transmission electric microscope, the phagosomes were replaced by vacuoles and the number of microvilli was reduced in EMB-treated cells. Animal experiments also demonstrated the vacuole formation within RPE of the EMB-treated rats. On the other hand, by in vitro phagocytosis assay using rod outer segment (ROS) as the target, we found EMB suppressed phagocytosis in the cultured RPE, which is consistent with the decreased rhodopsin uptake in the RPE of the EMB-treated rats. Furthermore, inhibitor of protein kinase C but not MAPK, prevented the EMB-induced phenotypical changes. Using a non-radioactive PKC assay, we also demonstrated the PKC activity in both RPE cell lines can be induced by EMB. In conclusion, EMB may exert toxic effects in RPE including suppression of cell growth, formation of cytoplasmic vacuoles and reduction of phagocytic functions via PKC signal pathway.





Questions about the HSR&D website? Email the Web Team.

Any health information on this website is strictly for informational purposes and is not intended as medical advice. It should not be used to diagnose or treat any condition.