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Abstract

Vanadium has recently been reported to induce interphase and M-phase (mitotic) programmed cell death via the generation of hydroxyl free radicals (OH*). In this paper, the effects of antioxidants on: (a) vanadyl[IV]-generated OH* free radical levels; and (b) cellular glutathione in vanadyl [IV]-treated Chang liver cells were evaluated. The surface morphology of vanadyl-treated mitotic cells was studied by confocal and scanning microscopy. The free radical scavengers zinc chloride, glucose and thiourea reduced the levels of vanadyl-induced OH* free radicals and partially prevented the depletion of cellular glutathione. Concurrent with OH* free radical production, vanadyl-treated telophase cells exhibited excessive cell blebbing and cell shrinkage. The morphological features demonstrated in vanadyl-induced mitotic programmed cell death as a consequence of oxidative stress is novel.

Increased Cytotoxicity of Vanadium to CHO-K1 Cells in the Presence of Inorganic Selenium

“…Nevertheless, we cannot exclude that it may involve Se-dependent disturbance of cellular detoxification of vanadium excess. Synergistic toxicity between selenite and vanadyl may also be attributed to increased oxidative stress, as both compounds tested are known for their prooxidant activities (Bay et al 1997 , Yang et al 2004 , Chung et al 2006 ).…”