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Iron Indices in Bottlenose Dolphins (Tursiops truncatus)

Author(s): Mazzaro, L.M.; S.P. Johnson; P.A. Fair; G. Bossart; K.P. Carlin; E.D. Jensen; C.R. Smith; G.A. Andrews; P.S. Chavey; S. Venn-Watson


Publication Type: Journal Article

Journal Title: Comparative Medicine

Date of Publication: 2012

Reference Information: 62(6): 508-515

Abstract: Bottlenose dolphins (Tursiops truncatus) can have iron overload (hemochromatosis), and it is believed that managed populations of dolphins may be more susceptible to this disease compared to wild dolphins. Serum iron, total iron binding capacity (TIBC), transferrin saturation (TS), and ferritin using a dolphin-specific ferritin enzyme linked immunosorbent assay (ELISA) were measured in 181 samples from 141 dolphins from two managed collections and two free-ranging populations. While no iron indices increased with age among free-ranging dolphins, managed collection dolphins had increasing ferritin with age. Dolphins from managed collections had higher iron, ferritin, and TS values compared to free-ranging dolphins. Dolphins with high serum iron (> 300 µg/dl) were more likely to have higher ferritin but not ceruloplasmin or haptoglobin, demonstrating that high iron is due to a true increase in total body iron. A time series study of four dolphins with hemochromatosis treated with phlebotomy demonstrated significant decreases in serum ferritin, iron, and TIBC when comparing pre- and post-treatment samples; TS initially decreased but returned to comparable pre-phlebotomy levels by six months post-treatment. Wild dolphins were 15 times more likely to have low serum iron (< 100 µg/dl) compared to managed collection dolphins and this was associated with lower haptoglobin. In conclusion, bottlenose dolphins in managed collections are more likely to have greater iron stores compared to free-ranging dolphins. Identifying why this occurs among some dolphin populations and not others may help treat hemochromatosis in dolphins and provide clues to causes of non-hereditary hemochromatosis in humans.