Objective： To investigate the effects of mycotoxin moniliformin （MON） on the metabolism of aggrecan and type 11 collagen in human chondrocytes in vitro and the relationship between MON and Kashin-Beck disease （KBD）. Methods： Human chondrocytes were isolated and cultured on bone matrix gelatin to form an artificial cartilage model in vitro with or without MON toxin. Cell viability was determined by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide （MTT） assay. The expression of aggrecan and type II collagen in the cartilage was determined using immunocytochemical staining. Results： MON toxin inhibited chondrocyte viability in dose-dependent and time-dependent manners. MON reduced aggrecan and type Ⅱ collagen syntheses in the tissue-engineered cartilage. MON also increased the expression of matrix metalloproteinase-1 （MMP-1）, MMP-13, BC4 epitopes, and CD44 in cartilages. However, the expression of 3B3（-） epitopes in cartilages was inhibited by MON. Selenium partially alleviated the damage of aggrecan induced by MON toxin. Conclusion： MON toxin promoted the catabolism of aggrecan and type II collagen in human chondrocytes.
An ZHANGJun-ling CAOBo YANGJing-hong CHENZeng-tie ZHANGSi-yuan LIQiang FUClare E. HUGNESBruce CATERSON
Objective: To investigate the possible effect of nivalenol on metabolism ofthe cultured chondrocytes and the protection of selenium. Methods: The quantitative analyses ofmetabolism in single- layer cultured chondrocytes were performed by biocliemical means and theimpairment of DNA was observed by both of the single cell microgel electrophoresis assay and theagarose gel electrophoresis assay. Results: In the media containing different concentrations ofnivalenol (0. 000 5-0. 020 0 mg/L), the amounts of DNA and proteoglycan in matrix of thechondrocytes were decreased. The syn-thesis of protein was reduced and the impairment of DNAdeteriorated with the increase of the concentrations of nivalenol in tlte given dose. When seleniumwas added into the media, the impairment by nivalenol was decreased. In the media containingdifferent concentrations of nivalenol, however, the lipid peroxidation of the chondrocytes was notaffected by nivalenol, yet the amount of lipid peroxides significantly declined. Conclusion:Nivalenol may evidently cause impairment of the chondrocytes when its concentrations are in thepresent experimental range. Selenium can protect cultured cliondrocytes, but cannot prevent theirDNA from being impaired.
