AI Article Synopsis
- DEGME, EGME, and their metabolite MAA have been linked to negative reproductive effects, prompting research into their impact on cartilage cell development (chondrogenesis).
- In lab experiments, all three substances reduced proteoglycan levels and cell growth at higher concentrations, but only MAA consistently showed stronger effects at lower doses.
- The study suggests that DEGME and EGME cause general toxicity, while MAA specifically triggers cell death through a process called mitochondrial-mediated apoptosis.
Article Abstract
Diethylene glycol monomethyl ether (DEGME), ethylene glycol monomethyl ether (EGME) and their common metabolite, methoxyacetic acid (MAA) have been associated with adverse reproductive effects. The objective of this research is to investigate the effects of DEGME, EGME and MAA on in vitro chondrogenesis and the mechanisms by which these effects occur. Micromass cultures were exposed to DEGME, EGME or MAA for 5 days and proteoglycan abundance and cell proliferation determined. Longer-term 9- and 14-day cultures were exposed to MAA and apoptosis analyzed. All three chemicals decreased proteoglycan abundance and cell proliferation at the highest dose tested (100 microL/mL). However, only MAA showed a dose-dependent effect for both parameters at 0.01, 10, and 100 microL/mL. Furthermore, micromass cultures show an increase in apoptotic cells which when treated with MAA suggest that cell death could result from induced apoptosis. These results suggest that effects of DEGME and EGME are the result of generalized toxicity, but their metabolite MAA induces mitochondrial-mediated apoptosis during in vitro chondrogenesis.
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| http://dx.doi.org/10.1016/j.reprotox.2006.05.005 | DOI Listing |
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