Abstract
There is much literature on the toxic effects of anesthetics. This paper deals with both the volatiles and locals. Adverse effects appear to be multifaceted, with the focus on radicals, oxidative stress (OS), and electron transfer (ET). ET functionalities involved are quinone, iminoquinone, conjugated iminium, and nitrone. The non-ET routes involving radicals and OS apparently pertain to haloalkanes and ethers. Beneficial effects of antioxidants, evidently countering OS, are reported. Knowledge at the molecular level should aid in devising strategies to combat the adverse effects.
Highlights
Toxic effects are a common response to many physiologically active substances including anesthetics
electron transfer (ET) results in interference with normal electrical effects, such as that which occurs in respiration or neurochemistry
The ether was found to undergo an oxygen uptake in rat liver microsomal membrane [23]. These observations are in line with the oxidative metabolism outlined in Scheme 2 which entails initial conversion to a carbon radical followed by oxidation to hydroperoxide with decomposition to the metabolites
Summary
Toxic effects are a common response to many physiologically active substances including anesthetics. Two pathways appear to be involved, namely, formation of reactive oxygen species (ROS), by redox cycling and electron transfer (ET), and ROS generation by non-ET routes. The latter pathway pertains to haloalkanes, ethers, and ethanol, whereas the former includes propofol, midazolam, and ketamine. The preponderance of bioactive substances or their metabolites incorporates ET functionalities, which, we believe, play an important role in physiological responses, examples of which include the following: quinones (or phenolic precursors), metal complexes (or complexors), nitroso and hydroxylamine metabolites from ArNO2 and ArNH2 [1], and conjugated imines (or iminium species). There is brief discussion of other toxic modes of action for anesthetics
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