Exposure to low-level chemicals and ionizing radiation: reactive oxygen species and cellular pathways

Abstract

<jats:p> Reactive oxygen species (ROS), which contribute to the energy landscapes in and around cells, play numerous roles in maintaining normal cell homeostasis as components of signaling pathways. Excessively high levels of ROS, on the other hand, can lead to pronounced DNA damage and a variety of cellular responses, including cell cycle arrests, senescence, apoptosis and possibly cancer. Far less is known, however, about how supra-basal levels of ROS that can be generated in response to low doses of ionizing radiation or chemicals in the environment may bring about untoward or perhaps even beneficial cellular responses. Even so, some evidence suggests that adaptive responses that have been associated with ROS-generating stimuli can have protective effects by fundamentally altering subsequent cellular dose-response profiles to otherwise detrimental stresses. Yet, even these seemingly favorable ‘adaptive’ effects may have longer-term untoward consequences. Other effects that have been associated with supra-basal levels of ROS, such as enhanced states of cell proliferation, potentially could have a protective function. But again, such increases in cell growth, which may be accompanied by greater than normal ROS-mediated damage to DNA, as well may ultimately favour the expansion of cells with heritable mutations. Unfortunately, the state of the art of our current understanding of how elevated but still low-level increases in ROS that may be induced by environmental stimuli presently precluded incorporation of supra-basal ROS-associated mechanisms in predictive risk assessment models, both at the population level and at the level of individualized risk assessment. </jats:p>

Barium inhibits arsenic-mediated apoptotic cell death in human squamous cell carcinoma cells

“…4c) and NAC (data not shown) in HSC-5 cells. H2AX, a histone variant, is phosphorylated in response to ROSmediated DNA damage (Lehnert and Iyer 2002;Rogakou et al 1998). We conWrmed that arsenic-induced phosphorylation of H2AX, H2AX (lanes 1 and 2 in Fig.…”

On the interaction of non-thermal atmospheric pressure plasma with tissues

“…One possible mechanism underlying these effects is generation of reactive oxygen species ROS, which at low levels induces cell proliferation and at high levels induces cell death through DNA damage [14]. To determine whether DBD plasma treatment of cells induced DNA damage, we looked at phosphorylation of H2AX, a histone variant that is phosphorylated in response to DNA double strand breaks [15].…”

Stimulation of the Proliferation and Differentiation of Skin Cells by Ferrous Ferric Chloride from a Distance

“…In fact, low-level ionizing radiation has been shown to stimulate the cell proliferation, 15) or it may be that free electrons induce reduction reactions in the cells. It is also reported that carbon materials such as graphite and activated charcoal can cause the proliferation of certain bacteria over a distance of several centimeters.…”