Abstract
There is an increasing interest to identify plant-derived natural products with antitumor activities. In this work, we have studied the effects of aqueous leaf extracts from Amazonian Vismia and Piper species on human hepatocarcinoma cell toxicity. Results showed that, depending on the cell type, the plants displayed differential effects; thus, Vismia baccifera induced the selective killing of HepG2, while increasing cell growth of PLC-PRF and SK-HEP-1. In contrast, these two last cell lines were sensitive to the toxicity by Piper krukoffii and Piper putumayoense, while the Piperaceae did not affect HepG2 growth. All the extracts induced cytotoxicity to rat hepatoma McA-RH7777, but were innocuous (V. baccifera at concentrations < 75 µg/mL) or even protected cells from basal death (P. putumayoense) in primary cultures of rat hepatocytes. In every case, cytotoxicity was accompanied by an intracellular accumulation of reactive oxygen species (ROS). These results provide evidence for the anticancer activities of the studied plants on specific cell lines and suggest that cell killing could be mediated by ROS, thus involving mechanisms independent of the plants free radical scavenging activities. Results also support the use of these extracts of the Vismia and Piper genera with opposite effects as a model system to study the mechanisms of the antitumoral activity against different types of hepatocarcinoma.
Highlights
Cancer is a major cause of death worldwide and the liver cancer the third most common cause of cancer death [1]
In previous reports we described the content of total phenols and flavonoids, and the in vitro antioxidant activities of aqueous extracts from Colombian Amazonian plants prepared as infusions as are commonly used in traditional medicine [17,18]
We found that cytotoxicity to human and rat hepatoma cell lines was accompanied by a marked increase of the intracellular reactive oxygen species (ROS) production
Summary
Cancer is a major cause of death worldwide and the liver cancer the third most common cause of cancer death [1]. There are differences in the activity of drug metabolizing enzymes; hepatoma cells have negligible levels on various P450 cytochromes [8,9]. This lack of phase I enzymes makes tumor cells more tolerant to certain concentrations of drugs that generate toxicity in normal hepatocytes after they have been metabolized. These differential characteristics between cancer and normal cells could have clinical applications
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