Date of Award


Degree Type


University or Center

Atlanta University (AU)

Degree Name




First Advisor

Dr. Rosalyn M. Patterson

Second Advisor

Dr. Curtis L. Parker


The present study was conducted to determine the effects of dimethylsulfoxide (DMSO) on the differentiation of chick limb mesenchymal cells in vitro. Cells treated with 30 and 40 mg DMSO/ml of medium for 72 h were inhibited from producing cartilage. Chromosome aberrations were induced in cells treated with 1-5 mg DMSO for 24 h. The compound also induced alterations to the morphology of the cells such as reduction in the cell size and cytoplasm, cytoplasmic vacuolization and alterations to the plasma membrane and cellular organelles. There was also a decrease in cell density when the cells were exposed to DMSO for 48 and 72 h. To determine if the inhibition of cartilage production was related to alterations in macromolecular synthesis, cells were pulse-labelled with [3H]-thymidine, [3H]-leucine, [3H]-glucosamine and [35S]-sodium sulfate to,measure DNA synthesis, protein synthesis, hexose utilization and glycosaminoglycan (GAG) synthesis, respectively. Results indicated that 30 and 40 mg DMSO/ml of medium significantly reduces the synthesis of products in chick limb mesenchymal cells. There was also a reduction in the total DNA and protein content after a 48 and 72 h exposure to DMSO but the ratio of total protein content to total DNA content remained the same. There also appeared to be an increase in total GAG content following a 24 and 48 h exposure to 40 mg DMSO/ml Of medium. Immunofluorescence studies indicated that cells exposed to 30 and 40 mg DMSO/ml of medium retained fibronectin at the cell surface after 72 h in culture and the compound appeared to have altered the arrangement of actin filaments within the cells. These results suggest that the inhibition of chondrogenesis by DMSO may be related to a decrease in cell density, alterations in cellular morphology, macromolecular synthesis and the arrangement of actin filaments as well as the retention of fibronectin at the cell surface.

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