Retinoids in marine mammals and their use as biomarkers of organochlorine compounds

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A. Borrell
V. Tornero
A. Aguilar

Abstract

Retinoids, also known as vitamin A, are non-endogenous molecules that are essential for a number of physiological processes in mammals. Imbalance of retinoids has been associated with reproductive impairment, embryonic mortality, growth retardation and bone deformities, pathologies in skin and the nervous system, and immune suppression. Mammals cannot produce retinoids so their primary source is dietary. They are absorbed by the small intestine and packaged as retinyl esters in chylomicrons, which enter the circulation and end up mostly in the liver and fatty tissues. Plasma retinoid levels are homeostatically regulated, so they remain constant despite variations in dietary supply or tissue stores. Therefore body depletion of retinoids cannot be reliably assessed through levels in blood, and should be evaluated through concentrations in depot tissues. In marine mammals, the main storage sites for retinoids are liver and blubber. Although not a universal rule, the concentration of retinoids often increases with age in both sexes because of progressive build-up of retinyl esters. In addition, sex often affects retinoid levels, but the nature and magnitude of this effect varies between species and populations. Taxonomic, life-style (particularly dietary) and climatic differences may explain dissimilarities in the effect of age and sex on retinoid levels. For this reason, retinoids can be used to distinguish populations or population components showing distinct dietary, behavioural, or other traits. Disease, particularly when affecting organs of physiological importance or inducing malnutrition, may affect retinoid tissue levels, so care should be taken when studying concentrations in stranded animals. Organochlorine compounds, particularly PCBs, dioxin (TCDDs) and DDTs, increase mobilisation of retinoids from hepatic and extrahepatic storage sites into serum, accompanied by enhanced degradation and elimination of retinoids through urine. In terrestrial mammals, this effect increases retinoid concentration. Conversely, in some species of marine mammals plasma retinoid levels have been reported to decrease when exposure to organochlorines increases, although the physiological mechanisms are unclear. However, given the homeostatic regulation of retinoids in blood, variation in plasma is expected to be less than that in liver or blubber. Because retinoid tissue levels vary in marine mammals even at moderate exposure to organochlorines, and original levels are restored when such exposure decreases or disappears, retinoids may be used as a biomarker of the impact of pollutants on populations. Further research is needed to validate their use, particularly in cetaceans.

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