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SEMINAR: MBF602 9/23/11 S/A 103, 1:00pm Rachael Heuer: Ocean acidification leads to counterproductive intestinal base loss in the gulf toadfish (Opsanus beta)
| From: | "Maxine Williams" <mwilliams@rsmas.miami.edu> |
| Subject: | SEMINAR: MBF602 9/23/11 S/A 103, 1:00pm Rachael Heuer: Ocean acidification leads to counterproductive intestinal base loss in the gulf toadfish (Opsanus beta) |
| Date: | Wed, 21 Sep 2011 14:01:59 -0400 |
|
MBF602
9/23/11 S/A 103, 1:00pm Student Speaker Rachael Heuer Ocean
acidification leads to counterproductive intestinal base loss in the gulf
toadfish (Opsanus beta) Oceanic
CO2 has increased from 280 to 380ppm since pre-industrial times and
is expected to reach 1000 and 1900 ppm by 2100 and 2300, respectively. In
addition, levels up to 2300 ppm have been reported from upwelling zones. We
recently demonstrated that levels as low as 750 ppm induces acidosis in
toadfish, leading to compensation by retention of blood HCO3-
to defend pH. Since increases in serosal HCO3- increases
HCO3- secretion rates in isolated intestinal tissue, it
was hypothesized that elevation of blood HCO3-during
1900ppm CO2 exposure would increase base secretion rates in vivo.
Toadfish rectal fluids were measured for pH, osmotic pressure, ionic
composition, and total CO2. Precipitated CaCO3 from these
rectal fluids was analyzed for titratable alkalinity, Mg2+ and Ca2+
content. As hypothesized, toadfish exposed to 1900ppm exhibited higher rectal
base excretion rates, higher fluid [HCO3-] and lower
fluid [Cl-] than controls suggesting increased intestinal anion
exchange as a result of the compensated respiratory acidosis. This study
verifies that elevation of plasma HCO3- during exposure
to CO2 levels observed currently in certain regions and expected
globally over the next centuries, leads to greater intestinal HCO3-
loss, a process that acts against compensation for CO2 induced
acidosis. Rachael
Heuer University
of Florida, B.S. Zoology 2006 Entered
Ph.D. Program Fall 2010 |
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