According to the "two-hit" hypothesis, secondary insults that may severely damage the steatotic liver include reactive oxygen species, endotoxin, tumor necrosis factor-alpha (TNFα) and other cytokines (Day and James 1998).
These molecules include reactive oxygen species (ROS) and transported ions.
The functions of Cygb remain to be elucidated; however, it may include detoxification of reactive oxygen species (ROS) and scavenging NO [ 7, 8].
Such an association would provide evidence that RD in this population may include individuals with reactive arthritis (ReA) from deployment-related infectious gastroenteritis.
Associated findings of epididymo-orchitis may include skin thickening and reactive hydrocele [17].
Additionally, in advanced cases M. leprae infection causes specific osteological deformations in the areas of the nasal aperture, anterior nasal spine and alveolar process on the premaxilla, cortical areas of the tibia and fibula, distal ends of the metatarsals and diaphyses of the phalanges that may include both direct and reactive changes [6], [7], [8], [9], [10].
The putative biological mechanisms may include direct effects of reactive oxygen/nitrogen intermediates and TNFα released by the M1 macrophages in close proximity to the tumor cells, and/or indirect effects through activation and recruitment of cytotoxic T cells [ 15].
These radicals are unstable; the pathological consequences in the testis of these very reactive agents may include reduced sperm counts, disrupted hormone levels, impaired enzyme activities, and necrosis [8].
Potential toxicological consequences of excess iron may include production of free radicals and other reactive oxygen species.
There are a few mind-sets to avoid as well (side effects may include crashed aircraft and the Yom Kippur War): "cognitive tunneling," "reactive thinking," and an exaggerated disposition for "cognitive closure".
