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Cell Biology International (2007) 31, 24–29 (Printed in Great Britain)
Nitric oxide affects preimplantation embryonic development in a rotating wall vessel bioreactor simulating microgravity
Yu‑jing Caoa1, Xun‑jun Fanab1, Zheng Shena, Bao‑hua Maac and En‑kui Duana*
aState Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, 25 Beisihuan Xi Lu, Haidian, Beijing 100080, People's Republic of China
bGraduate School of the Chinese Academy of Sciences, 19 Yu-quan Road, Beijing 100039, People's Republic of China
cCollege of Animal Science and Technology, Northwest A&F University, 3 Taicheng Road, Yangling, Shaanxi 712100, People's Republic of China


Microgravity was simulated with a rotating wall vessel bioreactor (RWVB) in order to study its effect on pre-implantation embryonic development in mice. Three experimental groups were used: stationary control, rotational control and clinostat rotation. Three experiments were performed as follows. The first experiment showed that compared with the other two (control) groups, embryonic development was significantly retarded after 72h in the clinostat rotation group. The second experiment showed that more nitric oxide (NO) was produced in the culture medium in the clinostat rotation group after 72h (P<0.05), and the nitric oxide synthase (NOS) activity in this group was significantly higher than in the controls (P<0.01). In the third experiment, we studied apoptosis in the pre-implantation mouse embryos after 72h in culture and found that Annexin-V staining was negative in the normal (stationary and rotational control) embryos, but the developmentally retarded (clinostat rotation) embryos showed a strong green fluorescence. These results indicate that microgravity induced developmental retardation and cell apoptosis in the mouse embryos. We presume that these effects are related to the higher concentration of NO in the embryos under microgravity, which have cause cytotoxic consequences.

Key words: Simulated microgravity, Embryonic development, Nitric oxide, Nitric oxide synthase, Apoptosis.

1These authors contributed equally to this work.

*Corresponding author. Tel.: +86 10 6255 8112 (Off), +86 10 6263 1831 (Lab); fax: +86 10 6263 1831.

Received 9 February 2006/21 July 2006; accepted 4 September 2006


ISSN Print: 1065-6995
ISSN Electronic: 1095-8355
Published by Portland Press Limited on behalf of the International Federation for Cell Biology (IFCB)