Michael's salinity + metal pollution lectures Flashcards

1
Q

seawater

A

35ppt, not uniform across the world. Range = 28 - 37.

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2
Q

Hypersaline marine environments

A

> 35ppt all the way to 350 which is supersaturated (where salt actually comes out of the solution as salt precipitation).
-These areas are common in the northern hemisphere, especially in north America.
-Often occur in lagoons as salt pans.

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3
Q

Freshening + sea level rise

A

Some areas are becoming less saline as sea levels rise due to the melting ice sheets. This leads to reduced salinity and ocean freshening.
-And yet in some areas there is also salinity increase, predictions suggest it will go in two directions. The areas that are fresh will become more fresh, and the hypersaline areas will become more saline.

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4
Q

Water movements: osmosis

A

-Hypotonic = swollen cell, externally more dilute than within, so water moves in.
-Isotonic = normal cell, balanced net of water, balanced osmotic pressure
-Hypertonic = shrivelled cell, external solute levels are greater than within, water moves out

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5
Q

How do invertebrates respond in dilute sea water

A

-More dilute outside of cell than inside, so difference in osmotic pressure
-Ions move out, water moves in = swelling
-Also have extracellular space, external to the original cells
-In a dilute medium, the water goes in and the ions out
-But this is a problem for cells and the space around them
-This is why fresh and marine species can’t afford to mix, most organisms cannot stop this process

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6
Q

Osmoconformers

A

Extracellular osmotic pressure is always the same as the external osmotic pressure, with no regulation.
E.g., Antarctic nematode has some ability to keep internal osmotic pressure just above the isosmotic line. But not an ability to regulate upon decreased salinity. This is an osmoconformer response, they have no regulatory capacity.

Some organisms have the short-term ability for some regulation at low salinity but not long term, these organisms tend not to last long. These are called partial osmoregulators.

Other Osmoconformers, that aren’t good at regulating are; sponges, cnidarians, platyhelminths, some polychaetes, and some gastropods.

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7
Q

Behavioural ion regulation in an osmoconformer

A

-Lugworm lives in burrows, osmoconformer but bodily fluids don’t change with salinity
-Pump water through the burrow, and at low salinity they have reduced activity (so they don’t bring low salinity water into the burrow)
-This shows behavioural regulation as they adjust the salinity of water to 40% 2x a day
-When they are burrowed, they can offset the drastic changes in salinity by keeping osmolarity and ions the same.

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8
Q

Hyper-Iso-Regulators

A

Hyper = above
Tend to inhabit areas where salinity changes a lot, like estuarine or intertidal organisms. Iso = the same.
-They don’t conform at reduced salinity; they partially regulate so the internal concentration remains higher than the external (hyper).
-They switch to regulation at about 26 ppt.

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9
Q

Hyper-Hypo-Regulators

A

Hypo = bellow
-at full strength seawater their bodily fluid is lower than outside.
-In lower salinity, their body fluid is higher than the outside
-Organisms like this tend to have freshwater ancestors, due to evolutionary history

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10
Q

How to invertebrates osmoregulate in dilute seawater?

A

Problem = loss of ions + gain of water
-Extracellular = regulation is possible because of an increased uptake of ions by the gills or a specialised ion exchange surface. Or a decrease of permeability of outer covering. More common.
-Intracellular = regulation possible because of an increased exchange of ions between intra and extracellular space, or the accumulation of amino acids.
= Dilute seawater, reduce permeability, get more ions in.

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10
Q

Ion regulation

A

Good regulators until at low salinity

-Sodium is regulated via antennal gland (produces urine = water/ions), gill and gut. Maintain sodium at a higher level when water becomes more dilute.
-Magnesium is always low, via antennal gland, block gland to increases magnesium, tend to do it when they hibernate.
-Calcium is regulated via gills and gut when osmotic pressure declines, and is stored internally from food and blood as capsules
-Potassium is not regulated very well, falls off as osmotic pressure falls off (implications unknown)

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11
Q

Ion movements

A

Body fluid = similar to seawater in most inverts, but some ions are modified.

-K = similar to seawater except for squid. Na/K balance is important for action potential
-Mg = more variable + replaces Ca at the nerve endings, determines behaviour to some extent. MgCl used as anaesthetic in marine organisms sometimes.
-Ca = close to seawater except its higher in Ligia (semi-terrestrial), getting Ca for the exoskeleton in hard and is stored in gut and body fluid.

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12
Q

Ion movements: Donnan equilibrium

A

-Modifying effects of proteins
-Proteins are large and charged to exert osmotic pressure
-Tend to not get large protein concentrations outside of animals
-Will affect the balance of ions inside and outside

Largely similar mechanisms, not necessarily about the presence or absence of pumps. The difference seems to be how they use the pumps.

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13
Q

Hyporegulation in hypersaline conditions: brine shrimp

A

-Very good osmoregulators across their life cycle, they even have a salt larval gland
-All through gills basically in adult stage, when the gills are unable to function, they lose their ability to osmoregulate
-Regardless of their environment, they internal body fluids stay mostly constant

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14
Q

Ion movements

A

-Passive = Donnan equilibrium
-Active = ion transport in a dilute medium, otherwise risk of losing or taking too many on

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15
Q

Teleosts: marine

A

-Maintain an internal fluid osmotic pressure of 1/3 sea water strength
-They have problem of water moving out and salt moving in
-Their kidneys can’t concentrate ions either, its osmotic. They can make iso-osmotic
-They can’t drink more water since it also has ions
-They tend to excrete via ion pumps in the gills
-Don’t have the physiology for osmoregulation, they haven’t adapted like invertebrates

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15
Q

Teleosts: fresh

A

-Live towards the lower osmotic pressure, can’t survive in full strength sea water
-They internal body fluids have more ions than the surrounding sea water
-If they are in dilute water, the water will come in, cells will swell, and they will get some ions
-They drink less, if they need more ions though they pump them in through the gills
-Less costs than sea water because of the difference in osmotic pressure

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16
Q

Elasmobranchs: salt water

A

-Have an iso osmotic pressure closer to sea water
-They can also osmoregulate
-Ions are also 1/3 strength sea water, but they have more because they create urea internally in the tissues
-Their hearts work better in the presence of urea too (which is poisonous to humans)

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17
Q

Marine invertebrates

A

-Isosmotic so seawater is the same as the internal fluids
-They may retain the 1/3 seawater strength due to freshwater ancestors

18
Q

Effects of salinity on metabolism: osmoconformers

A

-Metabolism will tend to decline if a saltwater species enters freshwater
-If cells swell and burst their metabolism will slow or stop and they will probably die
-Metabolism may increase either side of an isosmotic point depending on the species
-There is a lower metabolic rate in freshwater, but in saltwater there is a slower metabolic rate at a higher salinity at one point.

19
Q

Effects of salinity on metabolism: osmoregulation

A

-May not be a single mechanism that underpins the metabolic responses to salinity, for example, locomotion, ion rations and hormone or enzyme disruption.
-There seems to be around 4 metabolic responses to fresh and saltwater changes. It’s very difficult to predict the responses due to a lack of data across species.

20
Q

Copper in the environment

A

A natural component of aquatic systems at low levels 0.1 ug L-1 in ocean water, 2.6ug L-1 in some estuaries.

Copper- an essential compound used in enzymatic reactions, important component of the respiratory pigment hemocyanin. So, some copper is needed, just not in excess. Copper also varies across freshwater and the sea.

21
Q

Pollution

A

Mining, agriculture antifouling paints. Thought to have been declining since 1980s in UK rivers but is still a concern since levels are close the thresholds for toxicity to occur.

22
Q

Toxicity

A

Tested by measuring mortality. In Carcinus maenas; 0.5mg L-1 – sublethal, majority of animals survive. 2 mg L-1 – lethal, mortality starts at day 4, 100% mortality by day 7.

23
Copper in water + gills
Copper is taken up through the gills, known site of damage is the gill epithelium. Can cause the thickening of the gill surface which leads to necrosis and damage at even 50ug L-1. Potential for internal hypoxia. Damage gill first, then main stress = internal hypoxia.
24
Concentration
Concentration- if concentration is too high, and the damage to great it can be lethal. Sub-lethal concentrations do less damage, and organisms have more ability to recover. -Lethal (D) = 2mg L-1, 5-6 days of reduced arterial oxygen, increased haemolymph lactate, and reduced pH. Basically, internal hypoxia. Within 18 days they died. -Sub-lethal (C) = 0.5mg L-1, 5-6 days of the same as the lethal does. If back to normal after 18 days, they can start recovery, but gills may remain damaged.
25
Cancer pagarus: John Spicer
-Acutely = arterial PO2 (how oxygenated is the haemolymph leaving the gill) is slightly but not significantly lower with copper, lactate accumulation. Thickened gill epithelium. Hit with hypoxia PaO2 (a = arterial blood) falls. -Chronic = recovery, copper concentration maintained, representing recovery while still exposed to pollutant.
26
Defence systems
-Metallothioneins (MT)- proteins that bind to metal to reduce the toxicity. -MT tends to be higher in gill tissues in more polluted sites, compared to clean sites.
27
Copper oxidative stress
-Can cause issues to the cells via oxidative stress, oxygen whilst essential can also be toxic to all marine life. It has to be handled carefully internally. -The majority of oxygen goes to the production of ATP. -There can be leaking electrons in the electron transport chain which can lead to ROS (reactive oxygen species) which are highly reactive and damage what ever they come into contact with (lipids, proteins, DNA). Three forms of ROS = Superoxide anion: O2 (radical oxygen, without an electron), Hydrogen peroxide: H2O2 (oxidant). Hydroxyl radical: OH (radical without an unpaired electron).
28
Antioxidants: mop up the ROS
-Enzymes like superoxide dismutase, catalase, glutathione peroxidase -Low weight metabolites like glutathione are cannon fodder for ROS that get used up by reacting with ROS -They basically offset ROS’s by turning them into water -Environmental conditions might increase ROS production to overwhelm defences causing oxidative stress -There is evidence of upregulation of antioxidants, particularly superoxide dismutase
29
Copper as a source of oxidative stress
-Cause increased production of hydroxyl radicals OH+
30
Stressors in the ocean
Most of the ocean experience >5 stressors, coastal environments experience >15 stressors. Most of the ocean >10 two-way stressor interactions. Spatial variations.
31
Stressors vary in space and time
-Different intensities, durations and changes in factors simultaneously or sequentially. -Together they can affect an organisms differently, perhaps some singular stressors don’t even affect organisms in the wild.
32
Multistressor approaches
-Historic data = geological records, correlate with current climate issues -Field based data = correlated multiple stressors against physiological performance -Lab based data = controlled manipulation of stressors, can identify the driving change
33
Lab: 2 stressor studies
-2x2 design, 2 stressors with 2 levels per stressor (control vs treated) Results can be grouped into three responses. If the stressor will add to the survival, it is called an antagonistic response, additive is where their combined effect is the sum of adding up their individual effects. If it is synergetic then the stressors together are worse together in combination than separate.
34
Synergistic response
Most common, then additive and then agnostic responses. Synergism is also known as ecological surprises since the stressors together are always worse than predicted. -May be false since the lab is not a natural environment, and don’t necessarily always have two stressors at the same time. -To make it more ecologically realistic we need to consider stressor order, timing and intensity. Sometimes applying the same concentration of pollutants in different orders changes the affect and the toxicity on the organism.
35
Stressor timings, Case Study: temp + salinity in tidepool sculpins
-First stressor followed by a recovery period before a second stressor -Pre-exposure to 12 degrees heat shock for 2 hours, then allowed to recover for different times from 0 to 48 hours. -Exposed to 2-hour osmotic shock, and measured percentage survival -Control = 32ppt, or 85pt -No recovery between stressors led to 100% synergistic response, and 100% mortality -8–48-hour recovery after heat shock, increased the tolerance of salinity (antagonistic response)! Protective effects began to wear off after 48 hours. -Mild stress may promote defences, responses to the first stressor may create a different starting point for the second stressor
36
Climate-driven hypoxia
Global oxygen decline by 2% since 1960, 227.4 petamoles. Further decline of 1-7% is predicted by 2100. Driven by temperature; reduced solubility, increased stratification, disrupted current systems, increased microbial oxygen consumption. -Hypoxia effects > warming and acidification -Will ocean warming lead to ocean deoxygenation? -Some evidence of hypoxia being the most deadly of the deadly trio, the effects of hypoxia are potentially amplified by other stressors
37
Collins et al. 2021: how does warming modify hypoxia tolerance?
-The metrics used for hypoxia tolerance -What will acute warming do to hypoxia tolerance? -How does long term warming modify hypoxia tolerance? Maybe the performance would stay reduced and they may be unable to recover
38
main indicators of hypoxia
-Pc, is the indicator of aerobic performance under hypoxia -Tolerance, which is the survival time or time to loss of equilibrium -Critical oxygen tension, if lower it means they are better at regulating oxygen levels, if higher it means they are time limited and not good at oxygen regulation. -Fish use LOE (loss of equilibrium), there comes a point where they don’t have enough oxygen to remain horizontal, and flip to become vertical.
39
Why might acute warming affect hypoxic responses?
-Temperature alone, ie normoxic conditions -Temperature speeds up metabolic rate and biochemical reactions = higher oxygen demand and harder to sustain, especially under hypoxia -Acute warming is detrimental to most taxa, it raises the SMR which can lead to a rise in Pc. -It reduces tolerance of severe hypoxia, which means it’s harder to meet energy demand and anaerobic energy stores are used much faster, accrue damage faster too
40
Does long-term warming allow some recovery?
-Long term warming induces different responses to acute warming due to acclimation -May have some mechanisms to reduce oxygen demand or increase oxygen supply -Partial acclimation happens in the long term as a partial response, aiding the organism in increasing the supply or decreasing demand.
41
Pc in fish
-Warm acclimation was benefit for 1 out of 6 fish species -Pcrit increases with temperature, reducing hypoxia tolerance due to oxygen demand -After a longer time at a high temperature, there is some recovery of the Pcrit by partial acclimatation There is no recovery of hypoxic performance under long term warning, they don’t seems to have any thermal acclimation capacity at all. Temperature increases their metabolism, and it stays like that. Most fish show more ability in adjusting their physiology.
42
LOE in fish
-Only 2 species of fish have been studied, showed improved tolerance under hypoxia after chronic warming through enhanced oxygen supply mechanisms -Acclimated animals tend to out-perform the acutely warmed individuals, showing some recovery in long-term warming, meaning they perform better when hypoxia hits. Probably due to oxygen supply mechanisms
43
Tolerance + survival time after warming in molluscs
Chronic warming improves performance in 1 out of 2 bivalve species, the mechanisms are unclear but probably due to the reduced accumulation of toxic end-products. Although as you increase temperature, hypoxia tolerance decreases.
44
Tolerance + survival time after warming in crustaceans
-When acutely warmed, their metabolic rate and critical oxygen tension increased, this leads to a reduced hypoxic performance -Increased Pcrit = decreased hypoxia tolerance, generally -Some were able to acclimate longer term and increase hypoxia performance somewhat Some species will do better, some will do worse and that will change in the long-term. This will shape ecology in the future
45
Will aquatic ectotherms perform worse under hypoxia and long-term warming?
-Acute warming is consistently detrimental for hypoxic performance -Chronic warming has no effect or partial improvement in performance for some species -There isn’t enough data with considerations to timing, so we are unable to predict what global warming will bring