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Impacts of UV radiation on marine biota

Impacts of Global Change on marine biota

Moira Llabrés Master of Global Change UMP-CSIC January 2010

INDEX

• 1. UV introduction

1.1. Concept and wavelengths 1.2. Factors influencing UV levels 1.3. Ozone history. Trends and global change

• 2. How do we measure UV radiation?

2.1. Instruments and units 2.2. UV index 2.3. UV penetration 2.4. Submarine UV levels

• 3. How UV affects marine organisms?

3.1. UV effects 3.2. Mechanisms to avoid UV and repair damage

• 4. Impacts of UV on marine organisms: a review
• 5. Some examples of UV studies

UV introduction

Electromagnetic radiation with a wavelength shorter than that of visible light, but longer than x-rays, in the range 100 nm to 400 nm UVR range UVC: 200-280 nm UVB: 280-315 nm UVA: 315-400 nm

UV introduction

UV radiation levels are influenced by:

1. SUN ELEVATION UV levels vary with time of day and time of year

• 2. LATITUDE

Highest UV levels closer to equatorial regions

• 3. CLOUD COVER

Scattering can have the same effect as the reflectance by different surfaces

• 4. ALTITUDE

At higher altitudes a thinner atmosphere absorbs less UV radiation

• 6. GROUND REFLECTION

UVR is reflected or scattered by different surfaces

• 5. OZONE

Absorbs part of UV. Ozone levels vary

• ver the year and even across the day

Ozone history

1970- Crutzen described that NO, increased with fertilizers, destroyed ozone 1974- Rowland & Molina indicated that CFC’s destroyed ozone 1985- Farman, Gardiner, Shankin published the Antarctic ozone hole (Nature)

Images and data courtesy NASA Ozone Hole Watch

Ozone loss in Antarctica

2009- 24 million km-2 2006 Record area: 26.6 million km -2 Ozone lost 4 DU year-1 between 1979-1995 (Weatherhead & Andersen 2006)

Ozone history

Font: http://jwocky.gsfc.nasa.gov/multi/multi.html)

Not only ozone loss was measured in Antarctica Ozone levels in Arosa (Switzerland) started to reduce in 1980

Ozone recovery predictions have been questioned because:

• Other substances able to destroy ozone (such as Nitrogen

dioxide, methane and water vapour) are being emitted

• Warming generated by Green house gases accumulation in the

atmosphere could be influencing the ozone recovery 1987- Montreal protocol got to stop the declining in stratospheric ozone

• levels. However, pre-1980 levels of ozone are not recovered yet

Actual predictions based on the rhythm of CFC’s disappearance from the atmosphere, indicate that pre-1980 ozone levels will not be recovered before 2050-2065 (Weatherhead & Andersen 2006) Ozone loss Increased UV-B radiation reaching marine ecosystems Ozone trends

Instruments and units How we measure UVR?

UV radiometers UV sensors

UV radiation units: W m-2 UV doses units: W s-1 m-2 equivalent to J m-2 as J = W s

Satellite data: ex. TOMS from NASA

TOMS: Total ozone mapping spectrometer ( http://toms.gsfc.nasa.gov/ery_)

UV index How we measure UVR? UVI measures the intensity of UVR rising the earth surface, in each wavelength, weighted to the potential human damage Global Solar UVI is formulated using the International Commission on illumination (CIE) reference action spectrum for UV-induced erythema on the human skin (ISO 17166:1999/CIE S007/E-1998)

Eλ is the solar spectral irradiance expressed in W m-2 nm-1 at wavelength λ dλ is the wavelength interval used in the summation Serλ is the erythema reference action spectrum Ker is a constant equal to 40 W m-2

UV index UV index shows the power of UV to produce damage in the skin As UVI varies depending of the latitude the WHO in collaboration with WMO, UNEP and ICNIRP created a standard system to measure UVI and presented it to the public with the following colour code:

WHO: World Health Organization WMO: World Meteorological Organization UNEP: United Nations Environment Programme ICNIRP: International Commission on Non-Ionizing Radiation Protection

UVI: 1 equals to 25 mW m-2

UVI values

UV penetration

Kd = KW + KP + KD

KW = attenuation by pure water KP = attenuation by particles (phytoplankton and detritus) KD = attenuation by DOM

Penetration of UVR in the water column depends

DOM concentration and optical quality

It is measured by the diffuse attenuation coefficient (Kd)

Diffuse attenuation coefficient (Kd, m-1) is calculated from measurements of downwelling irradiance by fitting the following equation to irradiance versus depth data. Kd = ln (E0/Ez) / Z

Z: depth E0: irradiance at depth 0 Ez: irradiance at depth Z

Ez = E0 e (-Kd *Z)

UV data Eastern Sambo, FL Keys (2000)

Z10% corresponds to the depth where irradiance is attenuated to 10% of the value just beneath the surface. UV penetration

Some examples of Kd (m-1) UV penetration

Z10%

Font: Tedetti & Sempere 2006. Review

Submarine UV levels There are until few measurements of UV penetration in the Ocean because equipment used is recent and there are only few laboratories able to evaluate the submarine UV radiation Tropical waters

Surface UV irradiance during the day 26/05/03 26ºN 18ºW Atlantic

Font: Llabrés & Agustí 2006

Polar waters Submarine UV levels

10 20 30 40 50 60 0,02 0,04 0,06 0,08 0,1 0,12 0,14

100 1140 1320 1500 1640 1820 2000 2140 305 313 320 340 380 395 PAR Radiación UV (!W cm-2 nm-1)

PAR (!mol fotones cm-2 s-1)

Hora local (h)

Surface UV irradiance during the day 16/01/04. Spanish Antarctic Base (Livingston Island)

Font: Llabrés & Agustí

Polar waters

Font: Agustí et al. ICEPOS-2005

Submarine UV levels UV penetration

UV effects on marine organisms

Direct UV effects

Photosynthetic inhibition and growth DNA damage Fish skin and ocular damage Phytoplankton mortality Loss of motility and orientation Deficient nutrient uptake Mortality of invertebrate larvae and eggs MAAs formation Denature proteins and pigments

UV effects on marine organisms UV induces chemical alterations in DNA bases generating photoproducts known as CPD (cyclobutane pyrimidine dimers), in which we have bindings of adjacent pyrimidine dimers.

DNA damage

UV denature DNA molecules which induces failures in replication and consequent genetic mutations CPD formation in Plankton & ice algae Seagrasses and macroalgae Invertebrates and fish eggs and larvae

UV effects on marine organisms

Indirect UV effects Oxidative stress: ROS formation

• UV reacts with DOM and other chemical compounds

such as nitrate inducing reactive oxygen species (ROS)

• ROS such as hydroxyl radical (OH-) and hydrogen

peroxide (H2O2) are toxic because react with biomolecules (proteins, lipids, DNA) modifying and destroying them. ROS cause lipid peroxidation of cell membranes.

• ROS can be formed in the water and inside organisms

cells

Mechanisms to avoid UV

Photoprotection systems

* Cell structures or parasols

• Mucus segregated from microalgae
• Special cell walls with glass formations

to reflect UVR as coccolithophores * Chemical substances which absorb UVR

• Mycosporines (MAAS), aminoacids only produced by

bacteria, fungi and algae

• Pigments as scytomenine produced by ice algae or

melanine synthesized by zooplancton organisms * Antioxidants which neutralize the toxic effect of ROS

• Ascorbate, cleaning enzymes and carotenoids
• Carotenoids only synthesized by photosynthetic organisms

Mechanisms to avoid UV

Photorepair systems

* DNA repair system

• Photoreactivation: stimulated by blue light and UV.

Enzymes as photolyases identifies CPD’s and repair bases

• Dark repair- acts without light. Enzymes identify the

damaged DNA zone, cut, synthetize the correct sequence and stick it in the damaged zone, cutting the damaged sequence * Protein repair system Systems which are present in all kind of cells and are very important in mammals cells. Ex. Human cell suffers 500000 lesions/day in DNA molecule

Acute impacts of elevated UV radiation on marine biota: a metaanalysis

Moira Llabrés, Susana Agustí, Miriam Fernández, Antonio Canepa, Francisco Vidal, Felipe Maurin, Carlos Duarte

LINC-GLOBAL (PUC-CSIC) IMEDEA (CSIC-UIB) ECIM, PUC

Although potential impacts of elevated UVB were experimentally assessed on marine biota in the past, a full quantitative assessment of the magnitude of these impacts was still pending

• a meta‐analysis of the published literature on experimental

assessments of responses of marine organisms to increased and reduced UV

• Assessing the magnitude of these responses
• Quantifying the response of various taxa and processes to elevated

UV To quantify the effects and relative sensitivity to UVB of marine

• rganisms and processes to allow incorporation of elevated UVB

levels in assessments of the response of marine biota to global change By

UV impacts Objective

1. Search of literature using Web of Science and Scholar Google 2. Database was performed using the following parameters: Specie Taxa Size Hemisphere origin: North or South Year Stage: adult or immature Function: Mortality Growth Metabolism Cellular-Molecular Demography Behaviour

Mortality rate Survival as % was converted to using

Methods

UV impacts

Methods

• the ambient UVR the organisms were growing on
• the UVR in the experimental conditions

UV levels Type of experiments

CONTROL condition : THAT where the organisms were exposed to the ambient solar radiation in their habitat (a) Experiments that partially or totally reduce UVB radiation relative to that received by the organisms in their habitat Using UVB‐opaque materials Transplanting organisms to deeper layers with reduced incident UVBR (b) Experiments that increased UVB radiation using artificial illumination with UV lamps Transplanting organisms to shallower depths

Methods

UV rel > 1 indicate experiments where UV was elevated relative to ambient values UV rel < 1 indicate experiments where UV was reduced relative to ambient values UV levels To allow comparisons between organisms growing across different incident ambient UV levels we used: the relative change in UV radiation in the experimental treatments (UV treatment) relative to the control (UV control) as the ratio: UV relative

Methods

Effect size: calculated as the ratio of the response variable in the treatment relative to that in the control

Effect Size > 1: adverse effects on organisms Effect Size < 1: improved

• rganism performance

Response traits that indicate stress (i.e. Mortality) ES= treatment/control Response traits that signal improved performance (i.e. growth) ES= control / treatment Null hypothesis: ES =1 Will be rejected if ES is significantly <1 when UVrel <1, signaling an improvement in organismal performance ES is significantly >1 when UVrel >1, signaling adverse effect on organisms

Results

Summary of the experiments analyzed

Most of experiments assessing the response to reduced UVR

76% 24 %

Fewer studies assessing the effects

• f increase UVR

Results

Mortality – greatest overall sensitivity to increased and reduced UVR

UV reduced UV enhanced Effect size Mortality rates across taxa are reduced by half when UVB radiation is reduced, and are increased by 3 times when UVB is enhanced

Results

Strong relationship between extent of biological responses and changes in UV relative to ambient values across taxa and functions

UV relative Effect size

Functions Taxa

A Slope =1 indicates biological response is proportional to that in UV Slopes >1 and <1 indicate biological response amplifies or buffers the change in UV Slope of the fitted relationships between effect size and relative UV radiation provides a parametrization of the sensitivity of organisms to UVR if significantly differs from 0

Early life stages were more vulnerable to increased UVB than adult organisms, as the slope of the relationship between Effect Size and the relative UVB was steeper for early life stages than for adults across taxa (0.88 vs. 0.71, respectively; ANCOVA, t-test) Organisms from the Southern Hemisphere, which in general support a greater UVB radiation for a given latitude than those in the Northern Hemisphere were significantly more resistant to increased UVB radiation than those from the Northern Hemisphere, as the slope of the relationship between Effect Size and the relative UVB was steeper for organisms in the Northern Hemisphere compared to those in the Southern Hemisphere (0.83 vs. 0.66, respectively; ANCOVA, t-test, p < 0.001)

Expected impacts of the increased UVB on marine biota, assuming a 1:1 relationship between changes in ozone (DU units) and incident UVB levels McKenzie et al. 1999 should result in mortality rates increased, across taxa of 25- Southern Ocean 5 % - Subtropical regions 10% – Arctic Knowing that the decline in ozone levels from 1970 to 1995 Weatherhead &

Andersen, 2006 was:

Using the relationships between Effect Size and Relative UVB levels described AND 3.2 % year-1 - Southern Ocean 0.7 to 0.8 % year-1- Subtropical regions 1.9 % year-1 – Arctic

These results are consistent with the widespread decline of marine biota since the 1970’s, suggesting that elevated UVB levels must be considered as a possible driver of these declines.

Krill, which has been shown to be highly vulnerable to increased UVB radiation (30), declined 60 fold in abundance in the Southern Ocean between 1970 and 2003(29), consistent with the greatly increased UVB radiation over the Southern Ocean. The Canadian cod stock, which eggs and larvae float near the sea surface (31), collapsed in the late 1980’s and failed to recover despite a moratorium (32), also in agreement with their high vulnerability to increased UVB levels (33, 34). The decline of corals in the tropics and subtropics is also consistent with increased UVB levels, as the results presented here show that they rank amongst the most vulnerable organisms to UVB. Moreover, corals experienced widespread mortality in 1997-1998 (35), an event that was attributable to the effects of El Niño (36), but which may have also involved elevated UVB levels since the summer of 1998–99 experienced one of the highest UV radiation recorded so far over the Southern Hemisphere(17). Oceanic primary production has also declined (37) and the least productive areas of the ocean expanded (38), consistent with the high mortality induced by UV radiation in the clear waters of the oligotrophic ocean (11, 12, 24).

The analysis shows that marine biota are highly vulnerable to UVB radiation, and that the significant increase in incident UVB radiation with deterioration of the ozone layer must have severely impacted on marine biota, greatly increasing mortality rates, with corals as well as fish eggs and larvae being the most sensitive

Some examples of UVR effects on phytoplankton organisms

Phytoplankton organisms

Pico-phytoplankton 0.2-2 µm Prochlorococcus sp. Synechocococcus sp. Picoeucaryotes Nano & microphytoplankton 2-200 µm Diatoms and flagellates Photosynthetic organisms dominant in the Oceans

4 experiments

• St. 14
• St. 32
• St. 42
• St. 66

20 m 5 m

Allows all radiation to pass through (UVR+PAR) Filters UVR+PAR

Glass Quartz

Filters most UVR

Dark

Picophytoplankton abundance

200 400 600 800 1000 200 400 600 800 1000 FL3-H SSC-H

Prochlorococcus Synechococcus Picoeucaryotes Beads

Flow cytometry

Parameters determined:

• Abundance and viability of picophytoplankton cells
• Daily UVR and PAR doses received by the samples in the

experiments

• Half-life times (T1/2) and lethal radiation doses (LRD50) for

Prochlorococcus sp., Synechococcus sp., and picoeukaryotes k (h-1): decay rate of cell abundance with time T1/2 = ln 2/ k LRD50,( kJ m-2) calculated from the previous equation in which k (h-1) is the decay rate on cell abundance with radiation doses

Local time (h)

Living cell concentration

Prochlorococcus Synechococcus

St 14 St 32 Fast cell mortality of Prochlorococcus exposed to total solar radiation with living cell abundance falling below detection limits after short exposures of 4 hours (at 100 and 57% treatments) and 6 hours (at 23% treatments)

Prochlorococcus sp. % Living cells

I- Initial values 0- 0% irradiance 23- 23% irradiance 57- 57% irradiance 100- 100% irradiance Strong mortality in all treatments exposed to UVR+PAR High mortality in 100 % and 57 % treatments exposed to PAR

Synechococcus sp. % Living cells No mortality was induced in experiment 1 High mortality in all treatments exposed to UVR+PAR No mortality was induced under PAR exposure

Picoeukaryotes % Living cells Mortality was also induced in picoeukaryotes in some treatments of the experiments

Cell decay rates for living cells of Atlantic Cell decay rates for living cells of Atlantic pico-phytoplanktonic pico-phytoplanktonic communities induced communities induced by total solar radiation and PAR radiation by total solar radiation and PAR radiation

Half-life times (h) Time estimated to reduced populations to 50% Prochlorococcus Synechococcus Picoeucariotas % Radiación UVR+PAR PAR UVR+PAR PAR UVR+PAR PAR 100 1.7-6.2 1.6-! 10.5 - ! 32.8-! 2.1-9.7 3.15-65.8 57 1.5-2.9 1.5-! 14.7 - ! 39.8-! 2.8-11.7 30.7-! 23 2.1-13.4 3.2-! ! ! 4.2-31.7 ! UVR LRD 50 (KJ m-2) UV doses needed to reduce populations to 50%

Prochlorococcus Synechococcus Picoeucariotas 320 ± 169 > 539 755 ± 311

More resistant

Impacts of UV irradiance on growth, cell death and the standing stock of Antarctic phytoplankton

Llabrés M. & Agustí S., AME in press

ICEPOS-1 (2004) ICEPOS-2 (2005) RV Bio-Hesperides

5 EXPERIMENTS

Spanish Antarctic Base Juan Carlos I (Livingston Island) Water sampling

South Bay (Livingston Island) Exp. 2, 3 Foster Bay (Decepcion Island) Exp. 1 Antarctic Peninsula. Exp. 4, 5 64º 44’S, 65º 42’ W--- 64º 03’S, 55º 50’W

Surface water

Chlorophyll a Phytoplankton abundance (epifluorescence microscope)

Sampling every 2 days

Phytoplankton cell death (Cell digestion assay, CDA)

T0 and Tfinal

Net growth rates Inhibition percentages

Sensor UV: CUV3 Solar UVR measurements ICEPOS-1

Metereological station at the spanish base

ICEPOS-2

Metereological station at the bridge

Sensor UV: UV6490

30 min integrated measurements Radiation measurements transformed to daily lethal radiation doses (KJ m-2d-1) Incubation Polycarbonate Quartz UVR filtered Allowed UVR+PAR to pass through 2 L 2 L

Days January-February 2004

10 20 30 40 50 60 70 80 ICEPOS-1 18 20 22 24 26 28 30 1 12 14 16

Days of February 2005

10 20 30 40 50 60 70 80 ICEPOS-2 7 9 11 13 15 17 19 19 21

3 m i n . i n t e g r a t e d U V R ( K J m

• 2

) Higher UVR levels in ICEPOS-1 than in ICEPOS-2 Averaged daily UVR doses ICEPOS-1: 584 KJ m-2 d-1 ICEPOS-2: 232 KJ m-2 d-1

UVR levels

Clorophyll a (µg l-1) High chl a values

• f 15- 25 µg l-1 in

treatments without UVR Values below 5 µg L-1 in UVR treatments Moderated response in ICEPOS-2, chla maximum values of 8 µg l-1

5 10 15 20 25 2 4 6 8 10

• Exp. 3

5 10 15 1 2 3 4 5 6 7

UVR+PAR PAR

• Exp. 2

Time (days) ICEPOS-1

1 2 3 4 5 6 7 8 4 8 12 16

Exp.4

ICEPOS-2

1 2 3 4 5 2 4 6 8 10

• Exp. 5

Dominated by diatoms: Thalassiosira Eucampia Chaetoceros Fragillariopsis Pseudonitzschia Flagellates: Cryptophyceae Phaeocystis (free form)

what happened with the phytoplankton community composition?

And …

Growth rates (d-1)

% dead cells

Higher % dead cells in treatments exposed to total UVR respect to treatments without UVR

10 20 30 40 50 60 70

• Exp. 2
• Exp. 4
• Exp. 5

Diatoms

UVR+PAR PAR

10 20 30 40 50 60 70

• Exp. 2
• Exp. 4
• Exp. 5

Flagellates

80% biomass inhibition when averaged daily UV radiation doses are up to 450 KJ m-2d-1

Inhibition phytoplanton biomass Growth inhibition Cell death

% inhibition phytoplankton biomass

UV radiation (KJ m-2d-1)

Averaged UVR half-life(h) 3 ± 1 11 ± 5.7 8.8 ± 7.5 816 ± 412 1827 ± 913 Cell diameter size (µm) 0.6 1 2 5-15 20-40 Phytoplankton Community Prochlorococcus Synechococcus Pico-eukaryotes Flagellates Diatoms

Smaller phytoplankton organisms present shorter half-life times

Phytoplankton UV damage Indirect ROS formation, highly reactive and toxic, as OH- Direct Direct UV exposure which causes damage to molecular levels

O3 + h! "O2 + O (1D) H2O + O (1D) ! 2 OH

Oxidative stress

Duration exp: 0.5-2 days Sampling: 2.5-7 hours Abundance and viability of pico, nano and microphytoplankton Atmospheri c air

Peristaltic pump

Bubble treatments Controls

250 ml

Surface water

250 ml

OH OH concentration determination Changes in eriouglaucine absorbance at 620 nm (reacts with OH) Mili-Q + erioglaucine 0.01 mM

7 experiments

Atlantic Ocean Antarctic Ocean

Experiments Position Local time Maximum OH (mol L-1) Duration COCA-2 Atlantic Ocean 21ºN 25º 59’W 13:00 5.1 x10-16 30 h (1.2 d) BADE-2 Exp. 1 Atlantic Ocean 20º 1’N 19º 16’W 20:30 1.9 x 10-16 50.5 h (2.1 d) BADE-2 Exp. 2 Atlantic Ocean 20º 9’N 19º 5’W 15:00 1.8 x 10-17 12 h (0.5 d) BADE-2 Exp. 3 Atlantic Ocean 21º 47’N 26º 42’ 19:00 9.4 x 10-17 35 h (1.4 d) BADE-2 Exp. 4 Atlantic Ocean 23ºN 29º 23’W 19:00 8 x 10-17 11 h (0.45 d) BADE-2 Exp. 5 Atlantic Ocean 24º 35’N 31º 14’W 15:00 9.1 x 10-17 34.5 h (1.4 d) ICEPOS-2 Antarctic Ocean 62º 44’S 60º 32’W 16:15 2.4 x 10-16 44 h (1.8 d)

Radical OH-1 (mol L-1)

Reduction of phytoplankton cell concentration associated to OH peaks detected

Living cell concentration

C e l l c

• n

c e n t r a t i

• n

OH concentration (mol L-1) Negative relationship between phytoplankton concentration and OH radical concentration

20 40 60 80 100

Control Treatment

% Dead cells

Synechococcus COCA-2 Prochlorococcus COCA-2 Synechococcus BADE-2 Diatoms BADE-2 Flagellates > 5µ BADE-2 Flagellates < 5µ BADE-2 Diatoms ICEPOS-2 Flagellates ICEPOS-2

Higher % dead cells in treatment that under control condition

0.05 0.1 0.15

Prochlorococcus Diatoms Flagellates Synechococcus

D e c a y r a t e s ( h

• 1

)

Treatment with OH radicals

Again higher decay rates in picophytoplankton populations: : Synechococcus and Prochlorococcus

Differences in UV sensibility between phytoplankton

• rganisms

coud be determined by SIZE Sensibility to UV in pico-phytoplankton It coincides with García-Pichel predictions (1994) Prochlorococcus is the most vulnerable and the smallest one (< 1 µm) GENETIC COMPLEXITY Prochlorococcus genome lacks

• f important genes for DNA

reparation (Hess et al. 2001,

Dufresne et al. 2005)

Synechococcus can prevent photosystem II inhibition front UV and has genes for DNA repair