Meeting Abstract
P3.32 Thursday, Jan. 6 Elevated temperatures induce lipid peroxidation in cardiac muscle but not other tissues from Antarctic notothenioid fishes DEVOR, D.P.*; GRIM, J.M.; CROCKETT, E.L.; Ohio University, Athens; Ohio University, Athens; Ohio University, Athens dd163606@ohio.edu
Antarctic icefishes (Family Channichthyidae) are unique in lacking the oxygen carrier hemoglobin (Hb) in their blood. Some species of these fishes also do not express myoglobin (Mb) in the heart, a tissue in icefishes that is particularly rich in both mitochondria and lipids. These characteristics may make icefishes particularly vulnerable to the potentially damaging reactions associated with lipid peroxidation (LPO). We hypothesize that elevated temperatures will raise LPO to a greater extent in Antarctic icefishes than in their red-blooded relatives. We quantified malondialdehyde (MDA), a secondary product of LPO, in brain, pectoral, and cardiac muscles of two species of icefishes and two red-blooded notothenioids after exposure to their critical thermal maximum (CTMax). Hearts from both species of icefishes (Chaenocephalus aceratus and Chionodraco rastrospinosus) and the red-blooded species with the lowest hematocrit (Lepidonotothen kempi) had at least 1.3-fold higher MDA/g tissue in animals at their CTMax temperatures than in control animals held at ambient temperatures. Neither the heart from the red-blooded Notothenia coriiceps (the species with the highest hematocrit), nor pectoral muscle or brain from any species, showed any increase in malondialdehyde content following exposure to CTMax. These data indicate that LPO damage may contribute to thermal tolerance limits in icefishes and L. kempi. Supported by NSF-OPP 0741301.
