Mechanisms of tetrahydroxy-1, 4-benzoquinone toxicity to V79 cells: involvement of free radicals produced by its autoxidation

The toxicity of a polyhydroxy derivative of p-benzoquinone, tetrahydroxy-l,4-benzoquinone (THQ), was investigated in Chinese hamster ribroblasts (V79-M8 line). The fast oxidative degradation of THQ, yielding reactive oxygen species, allowed its use as a suitable tool to study the mechanisms of cell injury under oxidative stress. Toxicity of THQ to V79 cells was evaluated by measuring its inhibitory effects on cell growth and upon DNA synthesis rate. Complete prevention of both effects by catalase implicated hydrogen peroxide as the central key in the mechanism of THQ cytotoxicity. The roles of the primary oxidative product of THQ, rhodizonic acid (RDZ), as well as that of calcium, were investigated. The dependence of THQ on hydrogen peroxide for cytotoxicity, together with the possibility of iron chelation by RDZ, led us to propose an intracellular Fenton-type reaction as the mediator of THQ toxicity toward V79 cells. The understanding of THQ toxicity mechanisms can help to gain insights into the way structurally related physiological compounds, such as catechol derivatives, produce their toxic effects on target cells.

Bacterial chemistry. VI. Biological activities and cytotoxicity of 1, 3-dihydro-2H-indol-2-one derivatives

The biosynthetic pigment from Chromobacterium violaceum BB-78, 1,3-dihydro-2H-indol-2-one and its derivatives exhibit biological activities such as antimicrobial action, low hemolytic effects on red blood cells and in vitro trypanocide activity. A relatively high cytotoxicity on V-79 hamster fibroblast cells of the biosynthetic pigment was found, although with the methylol derivative the toxicity was almost eliminated. The methylol derivative exhibited similar toxicity as Nifurtimox, a known, commercial trypanocide compound