| Literature DB >> 19490880 |
Abstract
In line with the origin of life from the chemical world, biological mortality kinetics is suggested to originate from chemical decomposition kinetics described by the Arrhenius equation k = A*exp(-E/RT). Another chemical legacy of living bodies is that, by using the appropriate properties of their constituent molecules, they incorporate all their potencies, including adverse ones. In early evolution, acquiring an ability to use new molecules to increase disintegration barrier E might be associated with new adverse interactions, yielding products that might accumulate in organisms and compromise their viability. Thus, the main variable of the Arrhenius equation changed from T in chemistry to E in biology; mortality turned to rise exponentially as E declined with increasing age; and survivorship patterns turned to feature slow initial and fast late descent making the bulk of each finite cohort to expire within a short final period of its lifespan. Numerical modelling shows that such acquisition of new functions associated with faster functional decline may increase the efficiency of investing resources into progeny, in line with the antagonistic pleiotropy theory of ageing. Any evolved time trajectories of functional changes were translated into changes in mortality through exponent according to the generalised Gompertz-Makeham law mu = C(t)+Lambda*exp[-E(t)], which is reduced to the conventional form when E(t) = E0-gammat and C is constant. The proposed model explains the origin of the linear mid-age functional decline followed by its deceleration at later ages and the positive correlation between the initial vitality and the rate of ageing.Mesh:
Year: 2009 PMID: 19490880 DOI: 10.1016/j.jtbi.2009.01.009
Source DB: PubMed Journal: J Theor Biol ISSN: 0022-5193 Impact factor: 2.691