## 3 Results and Discussion
### Determination of Cell Viability in Various Cancer and Noncancer Cell Lines  
The cell viability assay of rice sprout extracts at 24 and 48 h was performed using a neutral red assay in various cell lines including HepG2, HCT116, SK-MEL-2, and Jurkat, which have never \begin{table}
\begin{tabular}{c c c} \hline \hline
**Test Compounds** & **Ages (days)** & **IC\({}_{50}\) (ug/mL) \(\pm\) SD** \\ \hline \multirow{3}{*}{BGR} & 5–7 & 271.2 \(\pm\) 13.1 \({}^{\mathrm{a}}\) \\  & 10–15 & 238.8 \(\pm\) 10.4 \({}^{\mathrm{a}}\) \\  & 20–25 & 231.1 \(\pm\) 12.9 \({}^{\mathrm{a}}\) \\ \hline \multirow{3}{*}{RD6} & 5–7 & 571.7 \(\pm\) 17.4 \({}^{\mathrm{b}}\) \\  & 10–15 & 575.8 \(\pm\) 38.2 \({}^{\mathrm{b}}\) \\  & 20–25 & 636.7 \(\pm\) 34.6 \({}^{\mathrm{c}}\) \\ \hline Gallic acid & - & 2.24 \(\pm\) 0.03 \\ \hline \end{tabular} Data are expressed as mean \(\pm\) SD from five replicates. Different letters indicate a significant difference between test compounds (\(p\) < 0.05).  
\end{table} 
Table 2: 1,1-Diphenyl-2-picrylhydrazanyl (DPPH) radical scavenging activity of rice sprout extracts. The half-maximal inhibitory concentration (IC\({}_{50}\)) is a measurement of the effectiveness of the extract in inhibiting DPPH radical. \begin{table}
\begin{tabular}{c c c c c} \hline \hline \multirow{3}{*}{**Rice Cultivars**} & \multirow{3}{*}{**Ages (days)**} & \multicolumn{3}{c}{**FRAP Power (mmole) Per Weight in Gram of Extract**} \\ \cline{3-5}  & & **100 ug/mL** & **200 ug/mL** & **1000 ug/mL** \\ \hline \multirow{3}{*}{BGR} & 5–7 & 0.79 \(\pm\) 0.0051 \({}^{\mathrm{c}}\) & 0.84 \(\pm\) 0.0068 \({}^{\mathrm{c}}\) & 1.28 \(\pm\) 0.015 \({}^{\mathrm{c}}\) \\  & 10–15 & 1.37 \(\pm\) 0.017 \({}^{\mathrm{c}}\) & 1.86 \(\pm\) 0.069 \({}^{\mathrm{a}}\) & 2.22 \(\pm\) 0.014 \({}^{\mathrm{a}}\) \\  & 20–25 & 1.28 \(\pm\) 0.011 \({}^{\mathrm{b}}\) & 1.61 \(\pm\) 0.115 \({}^{\mathrm{b}}\) & 1.58 \(\pm\) 0.0302 \({}^{\mathrm{b}}\) \\ \hline \multirow{3}{*}{RD6} & 5–7 & 0.73 \(\pm\) 0.004 \({}^{\mathrm{c}}\) & 0.76 \(\pm\) 0.0049 \({}^{\mathrm{d}}\) & 0.93 \(\pm\) 0.0083 \({}^{\mathrm{f}}\) \\  & 10–15 & 0.77 \(\pm\) 0.016 \({}^{\mathrm{d}}\) & 0.85 \(\pm\) 0.061 \({}^{\mathrm{c}}\) & 1.21 \(\pm\) 0.016 \({}^{\mathrm{d}}\) \\  & 20–25 & 0.  
been previously reported. Cisplatin, a standard anticancer drug, was used as a positive control [35]. Results showed that at 24 h cisplatin showed strong to low antiproliferation on HCTT116, SK-MEL-2, Jurkat, HepG2, and Vero, respectively (Table 4). At 24 h, Jurkat was the most sensitive cell line responding to BGR at all ages and RD6 at 10-15 days as indicated by the lowest IC\({}_{50}\) value. BGR at age 5-7, 10-15 and 20-25 days decreased cell viability of Jurkat with the respective IC\({}_{50}\) values of 206.2 \(\pm\) 15.1, 261.9 \(\pm\) 6.6, 438.6 \(\pm\) 11.6 \(\mu\)g/mL when compared to control (\(p\) < 0.0001). RD6 at 10-15 days reduced the cell viability of Jurkat cells (IC\({}_{50}\) value of 310.2 \(\pm\) 28.0 \(\mu\)g/mL) while the other ages of RD6 were inactive to Jurkat cells. HCTT116 was the second cell line upon which BGR exerted a low reduction of cell viability. BGR and RD6 extracts were inactive in HepG2, SK-MEL-2, and Vero cells at 24 h (Table 4). At 48 h, Jurkat was the most sensitive cell line responding to BGR following by HCTT116 and HepG2. BGR showed greater inhibition of cell viability at 48 h than those of 24 h. BGR at 5-7, 10-15 and 20-25 days inhibited cell viability of Jurkat cells with the respective IC\({}_{50}\) values of 67.62 \(\pm\) 6.8, 166.7 \(\pm\) 13.2, 136.4 \(\pm\) 4.9 \(\mu\)g/mL compared to the control (\(p\) < 0.05). HCTT116 and HepG2 displayed low sensitivity to BGR (\(p\) < 0.05). Both BGR and RD6 were inactive in SK-MEL-2 and Vero at 48 h (Table 4). Notably, BGR and RD6 were inactive to Vero cells at both 24 and 48 h.  
The selectivity index (SI) indicates selective inhibition of cancer cell viability of the tested compound in comparison to the noncancerous cells [34; 36].