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. Author manuscript; available in PMC: 2017 Jan 15.
Published in final edited form as: Biochem Pharmacol. 2015 Oct 22;100:1–11. doi: 10.1016/j.bcp.2015.10.003

Figure 2. Proposed mechanisms of oxidative stress from CWA/TIC exposure.

Figure 2

These agents produce both direct and indirect effects that lead to cellular events known to trigger oxidative stress. In addition to these effects, the agents produce tissue injuries that promote leukocyte influx. Activation of leukocytes is yet another source of ROS/RNS production that further promotes oxidative stress. All of these points in CWA/TIC pathways to tissue injury and damage are potential targets for intervention with antioxidant therapy.