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. 2018 Dec 15;10(12):539. doi: 10.3390/toxins10120539

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© 2018 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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A schematic diagram hypothesising the impact of venom on MetHb production. Haemolysis (the lysing of RBCs) by phospholipase A2 (PLA2) and other venom components is a common effect of snakebite envenoming. In a healthy human, the oxidation of Hb to MetHb is constantly combated by an enzyme, MetHb reductase. After certain venomous snakebites, this equilibrium is shifted in favour of MetHb, a toxic species that is also known to be pro-inflammatory. This shift may be a result of the ROS, which is generated as a metabolite of l-amino acid deamination [via l-amino acid oxidases (LAAO)] or lipid peroxidation (via PLA2) present in various venoms. The potential mechanisms for venom-induced changes in MetHb production are shown in the figure as dotted magenta lines.