Lethality of inappropriate plasma exposure on chicken embryonic development
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Jiao Jiao Zhang1, Jin Oh Jo2, Do Luong Huynh1, Mrinmoy Ghosh1, Nameun Kim1, Sang Baek Lee2, Hak Kyo Lee3, Young Sun Mok2, Taeho Kwon4 and Dong Kee Jeong1,4
1Department of Animal Biotechnology and Advance Next Generation Convergence Technology, Jeju National University, Jeju, Republic of Korea
2Department of Chemical and Biological Engineering, Jeju National University, Jeju, Republic of Korea
3Department of Animal Biotechnology, Chonbuk National University, Jeonju, Republic of Korea
4Laboratory of Animal Genetic Engineering and Stem Cell Biology, Subtropical/Tropical Organism Gene Bank, Jeju National University, Jeju, Republic of Korea
Dong Kee Jeong, email: firstname.lastname@example.org
Taeho Kwon, email: email@example.com
Young Sun Mok, email: firstname.lastname@example.org
Keywords: non-thermal DBD plasma, chicken embryo, ROS, NRF2, ATP
Received: July 04, 2017 Accepted: September 03, 2017 Published: September 20, 2017
In this study, we examined the effects of non-thermal dielectric barrier discharge plasma on embryonic development in chicken eggs in order to determine the optimal level of plasma exposure for the promotion of embryonic growth. We exposed developing chicken embryos at either Hamburger-Hamilton (HH) stage 04 or HH 20 to plasma at voltages of 11.7 kV to 27.6 kV. Our results show exposure at 11.7 kV for 1 min promoted chicken embryonic development, but exposure to more duration and intensity of plasma resulted in dose-dependent embryonic death and HH 20 stage embryos survive longer than those at stage HH 04. Furthermore, plasma exposure for 4 min increased the production of reactive oxygen species (ROS) and inactivated the nuclear factor erythroid 2-related factor 2 (NRF2)-antioxidant response signaling pathway, resulting in suppression of antioxidant enzymes in the skeletal muscle tissue of the dead embryos. We also found decreased levels of adenosine triphosphate production and reductions in the expression levels of several growth-related genes and proteins. These findings indicate that inappropriate plasma exposure causes dose-dependent embryonic death via excessive accumulation of ROS, NRF2-antioxidant signaling pathway disruption, and decreased growth factor expression.
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