This study was conducted to determine the effects of argon plasma on the growth of soybean [Glycine max (L.) Merr.] sprouts and investigate the regulation mechanism of energy metabolism. The germination and growth characteristics were modified by argon plasma at different potentials and exposure durations. Upon investigation, plasma treatment at 22.1 kV for 12 s maximized the germination and seedling growth of soybean, increasing the concentrations of soluble protein, antioxidant enzymes, and adenosine triphosphate (ATP) as well as up-regulating ATP a1, ATP a2, ATP b1, ATP b2, ATP b3, target of rapamycin (TOR), growth-regulating factor (GRF) 1–6, down-regulating ATP MI25 mRNA expression, and increasing the demethylation levels of the sequenced region of ATP a1, ATP b1, TOR, GRF 5, and GRF 6 of 6-day-old soybean sprouts. These observations indicate that argon plasma promotes soybean seed germination and sprout growth by regulating the demethylation levels of ATP, TOR, and GRF.

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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.

The quality of avian semen is an important economic trait in poultry production. The present study examines the in vitro effects of non-thermal dielectric barrier discharge plasma on chicken sperm to determine the plasma conditions that can produce the optimum sperm quality. Exposure to 11.7 kV of plasma for 20 s is found to produce maximum sperm motility by controlling the homeostasis of reactive oxygen species and boosting the release of adenosine triphosphate and respiratory enzyme activity in the mitochondria. However, prolonged exposure or further increase in plasma potential impairs the sperm quality in a time- and dose-dependent manner. Optimal plasma treatment of sperm results in upregulated mRNA and protein expression of antioxidant defense-related and energetic metabolism-related genes by increasing their demethylation levels. However, 27.6 kV of plasma exerts significant adverse effects. Thus, our findings indicate that appropriate plasma exposure conditions improve chicken sperm motility by regulating demethylation levels of genes involved in antioxidant defense and energetic metabolism.

Non-thermal plasma treatment is an emerging innovative technique with a wide range of biological applications. This study was conducted to investigate the effect of a non-thermal dielectric barrier discharge plasma technique on immature chicken Sertoli cell (SC) viability and the regulatory role of microRNA (miR)-7450. Results showed that plasma treatment increased SC apoptosis in a time- and dose-dependent manner. Plasma-induced SC apoptosis possibly resulted from the excess production of reactive oxygen species via the suppression of antioxidant defense systems and decreased cellular energy metabolism through the inhibition of adenosine triphosphate (ATP) release and respiratory enzyme activity in the mitochondria. In addition, plasma treatment downregulated miR-7450 expression and activated adenosine monophosphate-activated protein kinase α (AMPKα), which further inhibited mammalian target of rapamycin (mTOR) phosphorylation in SCs. A single-stranded synthetic miR-7450 antagomir disrupted mitochondrial membrane potential and decreased ATP level and mTOR phosphorylation by targeting the activation of AMPKα, which resulted in significant increases in SC lethality. A double-stranded synthetic miR-7450 agomir produced opposite effects on these parameters and ameliorated plasma-mediated apoptotic effects on SCs. Our findings suggest that miR-7450 is involved in the regulation of plasma-induced SC apoptosis through the activation of AMPKα and the further inhibition of mTOR signaling pathway.