## 4 Discussion
\begin{table}
\begin{tabular}{c c c c c c c c c c c} \hline \hline  & & \multicolumn{3}{c}{**L***} & \multicolumn{3}{c}{**a***} & \multicolumn{3}{c}{**b***} \\ \hline
**Groups** & **Measurement** & \begin{tabular}{c} **Median** \\ **(\(\pm\)SD)** \\ \end{tabular} & **min** & **max** & \
\begin{tabular}{c} **Median** \\ **(\(\pm\)SD)** \\ \end{tabular} & **min** & **max** &
\begin{tabular}{c} **Median** \\ **(\(\pm\)SD)** \\ \end{tabular} & **min** & **max** \\ \hline C & initial & 34.77 (\(\pm\)0.98) & 32.43 & 37.29 & 8.36 (\(\pm\)0.65) & 6.85 & 10.05 & 1.55 (\(\pm\)0.40) & 0.78 & 2.96 \\  & at 3 weeks & 35.10 (\(\pm\)1.10) & 32.81 & 37.55 & 8.25 (\(\pm\)0.66) & 6.65 & 9.73 & 1.46 (\(\pm\)0.44) & 0.63 & 2.98 \\ \hline LP & before & 34.26 (\(\pm\)0.82) & 32.51 & 36.44 & 8.22 (\(\pm\)0.60) & 7.13 & 10.04 & 1.39 (\(\pm\)0.28) & 0.58 & 2.29 \\  & after & 34.97 (\(\pm\)0.79) & 33.08 & 38.08 & 8.12 (\(\pm\)0.56) & 6.87 & 9.58 & 1.32 (\(\pm\)0.26) & 0.72 & 2.26 \\ \hline P1 & before & 32.74 (\(\pm\)1.07) & 30.55 & 35.75 & 8.03 (\(\pm\)0.59) & 6.02 & 9.97 & 0.91 (\(\pm\)0.22) & 0.29 & 1.62 \\  & after & 33.58 (\(\pm\)1.23) & 31.06 & 36.99 & 7.98 (\(\pm\)0.61) & 6.22 & 9.71 & 0.82 (\(\pm\)0.29) & 0.00 & 1.51 \\ \hline P6 & before & 32.95 (\(\pm\)1.02) & 30.70 & 36.03 & 8.23 (\(\pm\)0.60) & 7.07 & 9.49 & 0.98 (\(\pm\)0.30) & 0.38 & 1.78 \\  & after & 35.31 (\(\pm\)1.27) * & 31.75 & 39.94 & 8.80 (\(\pm\)0.65) * & 7.13 & 10.31 & 1.45 (\(\pm\)0.43) * & 0.33 & 2.48 \\ \hline \hline \end{tabular}  
* (lightness), a
* (redness-greenness), and b
* (yellowness-blueness) values before and after LP exposure and 120-min O\({}_{2}\) NTP treatments (P1 and P6). C represented the resin natural aging; (n = 12 samples per group, n = 12 measurements per resin samples); P6 showed a significant increase of lightness and a significant decrease of a
* and b
* color coordinates;
* significant difference according to Kruskal-Wallis and Wilcoxon rank sum tests (\(p<0.05\)).  
\end{table} 
Table 3: Color coordinates changes of resin in the evaluated groups. 2 \(\times\) 10\({}^{-5}\) mbar over 120 min. This pressure is lower compared to the pressure during O\({}_{2}\) plasma treatment (2.50 \(\times\) 10\({}^{-4}\) mbar). Hence, the results of low pressure on _C. albicans_ were probably overstated. Regarding O\({}_{2}\) NTP treatment in low pressure condition, a 120-min treatment led to a significant reduction (>6 log) of _C. albicans_ viability. Consequently, the antifungal activity was essentially due to the plasma process. The efficacy of the different atmospheric- and low-pressure plasma devices highlights the role of the various generated species during the plasma process. Different hypotheses involve essentially UVs, reactive oxygen and nitrogen species (RONS), ion and electron species [41; 42; 44; 54]. These species have enough energy to break covalent bonds and initiate various chemical reactions in _C. albicans_ cells. Thus, UVs are well known to damage DNA cells by dimerization of the thymine base [55; 56]. RONS cause photodesorption or etching of the cell wall, peroxidation of lipids and ergosterol, the latter being a critical sterol of the cell membrane [57]. This leads to an increase in membrane permeability favoring leakage of cytoplasm and intracellular components, and ultimately to lethal cellular damage [40; 53; 58; 59]. Our SEM images highlighted the rupture of the cell membrane and the leakage of intracellular components after a 120-min O\({}_{2}\) NTP, which is in accordance with the previous hypotheses. After NTP O\({}_{2}\) treatment, the reduction of _C. albicans_ viability was similar whatever the sample material. However, the results were less reproducible when _C. albicans_ was seeded on resin samples, which was probably due to the different affinity of _C. albicans_ for the two materials. Indeed, the SEM analyses highlighted that the contaminated glass surface was characterized by large areas of yeast monolayers and small clusters.