Evidence suggests that nanometals can cause a range of sublethal effects in fish including respiratory toxicity, disturbances to trace elements in tissues, inhibition of Na+K+-ATPase, and oxidative stress.
Since reactive oxygen species (ROS) were enhanced in infected fish (increased respiratory burst of circulating leukocytes) [ 12], it is a reasonable conservative strategy to reduce RNS to avoid detrimental effects to the host.
Its waxing and waning presence during a red tide may provide a partial explanation for anecdotal accounts of high toxigenic organism cell counts in the absence of pronounced fish kills or respiratory irritation, or of relatively low cell counts and reports of "respiratory irritation" (Fleming et al. 2005).
For example, initial reports of toxicity indicated by changes in tissue biochemistry in rainbow trout exposed to aqueous TiO2 NPs and SWCNTs appear now to have now been related to occlusion of fish gills and respiratory distress rather than NP absorption and direct toxicity in tissues.
This suggests that CPY is subject to loss processes from fish in addition to respiratory loss, the obvious process being metabolic biotransformation, but growth dilution and egestion may also apply.
These events often cause a noticeable change in the color and smell of natural water bodies and may be accompanied by highly visible fish kills or even respiratory distress in humans who inhale tiny, aerosol particles created by wind and waves.
Lungs, already present in fishes, became the main respiratory organs of terrestrial vertebrates.
Clearly, determining if geographic ranges of tropical reef fishes are associated with respiratory thermal sensitivity will require more detailed knowledge on the geographical ranges and thermal performance curves of these species.
