Thermodynamics of pharmacological action for electron-accepting compounds on activated or damaged cell in the context of Ling's model of the living cell

TL;DR

This paper models the thermodynamics of pharmacological actions on cells, focusing on how compounds affect cell states and recovery through ATP-mediated protein disaggregation, using Ling's cell model.

Contribution

It introduces a thermodynamic framework for understanding drug effects on cell states, emphasizing physical processes of cell recovery and damage.

Findings

ATP disaggregates proteins, aiding cell recovery.

Reduction of effective temperature correlates with healing.

Protein mobility decreases during treatment.

Abstract

The theory describing action of medicines explored in this paper is based on assumption that vital activity of the cell may be described in terms of the model of two states: resting state and excitation. According to available physiological data excitation state is dangerous for cell and may cause different pathological changes, including "conformational" diseases, due to protein aggregation. Normally, the excitation is completely reversible and the key role is played here by ATP (adenosine-5'-triphosphate) which disaggregates proteins of cytomatrix. The same effect ATP exerts during cell injury by eliciting a "healing" effect. Damage of cell structures we consider as "illness", whereas removal of pathological consequences caused by protein aggregation of any origin we will call "a cure". The latter is considered as physical process of cell recovering from excitation/injury to resting state, which is analyzed in terms of our generalized thermodynamics. "Cure" results in reduction of effective temperature of cell proteins due to binding intracellular water which is present in the cell at concentration of approximately 44 M. As a result of the sorption processes mobility of both water and proteins is greatly reduced, and the corresponding reduction of the effective temperature seen by us as a measure of treatment effect.