The lysosomal system of the hepatopancreatic digestive cell of the
mussel (Mytilus sp.) is critical in intracellular food degradation, toxic
responses and internal cellular turnover. Mathematical and numerical
models are developed to simulate the responses of this system to varying
conditions, dietary and toxicological. The model evolution encompasses:
inclusion of glycogen/lipid storage forms; extrapolation to include nitrogen
metabolism; development of rate of endocytosis and food signal; increased
functionality of endo/lysosomes; shift to protein/carbohydrate/lipid based
model; and the incorporation of the cost of normal Sanction and
replacement of damaged components. Control is asserted through control
of cytosolic concentrations: the intial assumption of constant carbon
concentration is shown to be unacceptable for later models. A control
algorithm is developed which regulates cell volume by the ratio of
proteinaceous material to energy forms.
Endocytosis is shown to be the main determinant behind routine
cellular behaviour. Observed phasic behaviour of the digestive tubules is
incorporated into the cellular behavioural pattern. A probability-based
model for the rate of endocytosis is developed.
Increased autophagy as the sole response to toxic injury is found to
be inadequate to explain observed responses. It is proposed to complement
this response with impairment of lysosomal efficiency to explain this
inadequacy. Toxic injury is implemented through an increase in the rates of
damage to cellular components. Within the lysosome this leads to a
reduction in the concentration of digestive enzymes inhibiting lysosomal
performance and, in conjunction with the enhanced autophagy due to
increased cytosolic damage, invoking the lysosomal swelling commonly
observed.
Date of Award | 2008 |
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Original language | English |
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Awarding Institution | |
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Mathematical modelling of hepatopancreatic digestive cell of the blue mussel
McVeigh, A. (Author). 2008
Student thesis: PhD