A. domesticus and humidity question.

Anyone know the scientific reason behind why high humidity kills off House crickets?

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  • edited November 18

    Hi JButera, -

    When CO2 builds up the cell membrane alters, negative charged ions build up inside that cell & ATP (cellular made energy) gets low from energy diverted toward putting protons out of that cell. This can involve the circulating haemolymph.

    Also the body surface spiracles connected to trachea which lead to neural ganglia and CO2 can also diffuse into neurons; which does not involve using haemolymph. There the CO2 can stall neuron resting potential leading to depolorized neurons in the ganglia.

    Old experimental CO2 amplification experiments on Acheta domesticus determined it (excessive CO2) led to neuro-endocrine problems, under sized tracheal growth, plus phases of reduced feed intake depending on it's age & time during an instar. Curiously, in another experiment, at high temperature (50°Celsius) Acheta domesticus lived longer when not given much oxygen as compared to when give 35% or 95% oxygen.

    What happens under 100% oxygen supply is that spiracles constrict and 90% less CO2 gets out. Most CO2 buffering is done by tissue cells & normally CO2 is quickly put out from tissues (& hemolymph). To get this rapid response at least some tissue should have the enzyme carbonic anhydr-ase & I wonder if Acheta domesticus gene copy number for this enzyme may (?) be less than some other insects.

    Which brings up the ratio of O2 to CO2, which exhibit different force (partial pressure) of action. Insects are such resilient survivors because holding on to CO2 and drawing down on O2 results in H2O staying inside their trachea longer & allays body dessication.

    Besides water issues oxygen O2 is in a sense problematic to cells because it can instigate "oxidative" damage & free radicals. Having moisture condensate in the trachea naturally helps keep O2 out, which likewise closing a spiracle opening does.

    Still O2 & CO2 gasses must be moved (ventilated); so as O2 taken up CO2 has to be stashed (buffered) in haemolymph & tissue cells. The dynamic of O2 uptake while CO2 being buffered allows the creation of negative pressure in the trachea interior.

    However, to get negative pressure in the trachea interior O2 oxygen there has to be O2 in the trachea to be used internally in order to create a gradient (negative pressure); dying insects can not sustain that gradient. When O2 uptake is occuring the negative pressure also translates into negative water (hydrostatic) pressure; without that excessive moisture would escape as vapor out of the trachea via open spiracles.

    Convection of O2 into an opening spiracle with negative pressure inside (that spiracle) is only an initial response. Once sufficient initial O2 enters to sustain the negative pressure inside a trachea the convection inward of O2 transitions to a diffussion (of O2).

    Meanwhile, as O2 intake continues this leads to a progressive reduction in the interior volume of a trachea; which can be explained by the negative pressure gradient inside the trachea leading to internal O2 uptake "sucking" in the trachea sides. This too keeps more CO2 inside the insect & not from being released (ventilated) out of the spiracle.

    What I am trying to show is that in your very high humidity A.domesticus mortality circumstances is that the high humidity water vapor creates a high moisture level inside their trachea & CO2 is soluble in water more readily than O2 is soluble in water the trachea. Which in effect makes it harder for a negative pressure gradient inside the spiracle to develop for ample O2 oxygen diffusion; even though O2 convection may occur at an open spiracle mousture in there makes it hard for a lot of O2 to move along.

    Then the cellular level of CO2 rises, the cellular level of O2 oxygen is low & conditions are essentially the same as if the spiracle were closed - namely elevated CO2 & decreased cellular pH. Yet the natural physiological response to high CO2 pressure & low O2 oxygen pressure provoking spiracle opening for O2 to come in does not play out as well.

    Because (in your high humidity scenario) excessive tracheal moisture (H2O) is both holding extra CO2 that is supposed be buffered inside tissue cells/haemolymph) & is also interfering with sustaining the negative pressure gradient O2 oxygen requires for diffusion that has been called "passive suction ventilation." Then the damaging events described in the 1st 2 paragraphs above occur.

  • Thanks gringojay, would you say death by asphyxiation, in layman's terms?

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