Application of first order rate kinetics to explain changes in bloom toxicity—the importance of understanding cell toxin quotas

Abstract

Cyanobacteria are oxygenic photosynthetic Gram-negative bacteria that can form potentially toxic blooms in eutrophic and slow flowing aquatic ecosystems. Bloom toxicity varies spatially and temporally, but understanding the mechanisms that drive these changes remains largely a mystery. Changes in bloom toxicity may result from changes in intracellular toxin pool sizes of cyanotoxins with differing molecular toxicities, and/or from changes in the cell concentrations of toxic and non-toxic cyanobacterial species or strains within bloom populations. We show here how first-order rate kinetics at the cellular level can be used to explain how environmental conditions drive changes in bloom toxicity at the ecological level. First order rate constants can be calculated for changes in cell concentration (μc: specific cell division rate) or the volumetric biomass concentration (μg: specific growth rate) between short time intervals throughout the cell cycle. Similar first order rate constants can be calculated for changes in nett volumetric cyanotoxin concentration (μtox: specific cyanotoxin production rate) over similar time intervals. How μc (or μg) covaries with μtox over the cell cycle shows conclusively when cyanotoxins are being produced and metabolised, and how the toxicity of cells change in response to environment stressors. When μtox/μc >1, cyanotoxin cell quotas increase and individual cells become more toxic because the nett cyanotoxin production rate is higher than the cell division rate. When μtox / μc =1, cell cyanotoxin quotas remains fixed because the nett cyanotoxin production rate matches the cell division rate. When μtox/μc <1, the cyanotoxin cell quota decreases because either the nett cyanotoxin production rate is lower than the cell division rate, or metabolic breakdown and/ or secretion of cyanotoxins is occurring. These fundamental equations describe cyanotoxin metabolism dynamics at the cellular level and provide the necessary physiological background to understand how environmental stressors drive changes in bloom toxicity.