There are four main physiological mechanism of heavy metal resistance:
(a) Inactivation,
(b) Impermeability,
(c) By- pass, and
(d) Altered target site(s).
On the other hand, earlier studies reported that fungi tend to survive heavy metal stress either by adaptation or mutation. Not only fungi but few algae such as Stigeoclonium tenue can grow in a zinc-rich effluent and showed slightly greater resistance under in vitro conditions due to possible adaptation.
Enzymic flavoprotein is believed to play a key role in the mercury detoxification system of many bacteria. Bacterial strains which additionally detoxify organomercurials possess another enzyme organomercurial lyase which cleaves the covalent carbon mercury bond to release Hg2+ which is then volatilized by the action of mercuric reductase.
Many plasmids responsible for heavy metal tolerance were reported in bacteria. Mediation of penicillinase plasmid in importing resistance to divalent metal ions of mercury and cadmium is reported in Staphylococcus aureus. It has been suggested that heavy metal resistances may have been selected in earlier times, and that they are merely carried along today for selection for antibiotic resistances.
In Tokyo in 1970s both heavy metal resistance and antibiotic resistance were found with high frequencies in Escherichia coli isolated from hospital patients, whereas heavy metal resistance determinants were found in E. coli from an industrially polluted river.
Selection occurs for resistances to both types of agents in the hospitals, but only for resistance to toxic heavy metals in the river environment. The major recent progress has consisted of the cloning and DNA sequence analysis of determinants for mercury, arsenic, cadmium, and tellurium resistance and the initial reports of still additional resistances.
