Effect of Stratospheric Ozone Depletion and Enhanced Ultraviolet Radiation on Marine Bacteria at Palmer Station, Antarctica in the Early Austral Spring

Abstract We investigated the interactions between ozone‐depleted air masses and subsequent changes in UVB on marine bacterial abundance and production at Palmer Station, Antarctica from September to November 1999. During periods of low total column ozone (TCO), bacterial cell concentrations declined...

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Bibliographic Details
Published in:Photochemistry and Photobiology
Main Authors: Pakulski, J. Dean, Kase, Jason P., Meador, Jarah A., Jeffrey, Wade H.
Format: Article in Journal/Newspaper
Language:English
Published: Wiley 2007
Subjects:
Online Access:http://dx.doi.org/10.1111/j.1751-1097.2007.00222.x
https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fj.1751-1097.2007.00222.x
https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1751-1097.2007.00222.x
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Summary:Abstract We investigated the interactions between ozone‐depleted air masses and subsequent changes in UVB on marine bacterial abundance and production at Palmer Station, Antarctica from September to November 1999. During periods of low total column ozone (TCO), bacterial cell concentrations declined by 57%. Photoinhibition of bacterial [ 3 H]‐leucine (Leu) and [ 3 H]‐thymidine (TdR) incorporation due to UVB was greatest during periods of low TCO in September and early October. During diel (∼28 h) exposure experiments, light treatment samples exhibited >75–100% inhibition of TdR incorporation by mid‐afternoon. Leu incorporation exhibited maximum inhibition (50–100%) at sunset and early evening hours. Leu and TdR incorporation in light treatment samples did not exhibit recovery during subsequent periods of darkness. Bacterial Leu and TdR incorporation rates were inversely related to Setlow Dose during a period of recovery from low TCO. These data further suggested a threshold exposure below which bacterial Leu and TdR incorporation recovered rapidly. Recovery of bacterial production after acute Setlow Dose exposures lagged recovery of TCO and was linearly related to TCO measured 2 days previously. This lag in recovery may have resulted from the energetically expensive repair of UVR‐induced DNA damage acquired during periods of low TCO.