Abstract
Black (cv. BGR) and white (cv. RD6) glutinous rice sprouts from fertilizer- and pesticide-free farm in Khon Kaen province, Thailand were investigated for antioxidation and antiproliferative activity. Three different ages of rice sprouts were collected and prepared as the extract. BGR exerted higher antioxidant capacity than RD6 based on total phenolic (TPC) and total anthocyanin contents (TAC), DPPH, and FRAP assays. BGR at 10–15 days contained the highest TPC (29.72 ± 1.42 mg gallic acid equivalent/g extract) and reducing power (2.22 ± 0.014 mmole FeSO4/g extract). BGR at 20–25 days contained the highest TAC (0.86 ± 0.096 equivalence of cyanidin-3-glucoside/g extract) and DPPH radical scavenging activity (IC50 = 231.09 ± 12.99 μg/mL). Antiproliferative activity of the extracts was evaluated in the human T-lymphocyte (Jurkat), hepatocellular carcinoma (HepG2), colorectal carcinoma (HCT116), melanoma (SK-MEL-2) and noncancerous cells (Vero) by neutral red assay. BGR showed the most selective antiproliferation against Jurkat cells, by inducing apoptosis, and caspase 3/7 activity. BGR at 200 μg/mL from all ages significantly decreased ROS using DCFH-DA and increased endogenous glutathione levels in Jurkat cells compared to the control (p < 0.05). The higher antiproliferation of BGR than RD6 was via its antioxidation capacity and attributed to its higher phenolic and anthocyanin contents. BGR sprout is a potential source of biologically active substances good for wellness and health benefits.
Highlights
Cancer is an uncontrollable cell growth developed into abnormal cells that can invade normal body tissue
Induction of cancer by nongenotoxic agents can occur in 2 ways; (i) induction of mutations during continual cell division through misrepair results in an initiated preneoplastic cell that may clonally expand to a neoplasm, and (ii) stimulation of the selective clonal growth of already spontaneously initiated cells [1]
Results showed that at 24 h cisplatin showed strong to low antiproliferation on HCTT116, SK-MEL-2, Jurkat, HepG2, and Vero, respectively (Table 4)
Summary
Cancer is an uncontrollable cell growth developed into abnormal cells that can invade normal body tissue. Cancer formation is the multiple steps involving the transformation of the normal cells into cancer cells (initiated cells), which undergo tumor promotion to become preneoplastic. Carcinogens induced cancer either through molecular targets or cellular effects involving genotoxic and nongenotoxic mechanisms. The genotoxic agent can damage genomic DNA resulting in mutation and clastogenic changes. The nongenotoxic agent alters gene expression and modulates cell growth and cell death. Induction of cancer by nongenotoxic agents can occur in 2 ways; (i) induction of mutations during continual cell division through misrepair results in an initiated preneoplastic cell that may clonally expand to a neoplasm, and (ii) stimulation of the selective clonal growth of already spontaneously initiated cells [1]
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