Author Type

Graduate Student

Date of Award

1991

Document Type

Thesis

Publication Status

Version of Record

Submission Date

October 2026

Thesis/Dissertation Advisor [Chair]

Hartmann, James X.

Abstract

It is not known by what mechanism members of the subclass Elasmobranchii derive their natural resistance to neoplasia. To determine if this resistance is at the cellular level, cultures of shark (Carcharinus falciformis) cells were exposed to varying concentrations of the chemical carcinogens methanesulfonic acid ethyl ester (EMS) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). Treated cells were assayed for cytotoxicity, formation of transformed foci and growth in agarose. It was found that a greater chemical concentration was necessary to reach LC50 in shark cells than in mammalian cells (BHK21 Cl13). Shark cell cultures developed no transformed foci over a range of chemical concentrations of EMS whereas foci formed at all concentrations in BHK control cultures exposed to EMS. Treated shark cells did not develop transformed colonies in agarose, but the mammalian cells readily formed colonies. These results suggest that the natural resistance of elasmobranchs to neoplasia could be partially, if not entirely, regulated at the cellular level.

Extent

47 p.

Comments

Charles E. Schmidt College of Science|Thesis (M.S.)--Florida Atlantic University, 1991.|Charles E. Schmidt College of Science

Identifier

FADT14708

Format

pdf

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