Chemical Interactions between Mercurial Species and Surface Biomolecules
175
considerations, one can envisage that heavy metal elements present a wide range
of activity on microbial cells, some biochemical effects, being described in the
literature concerning microbial metabolism of any structural change in the cells.
Another methylation mechanism described in the literature involves the
synthesis of metal alkyls related to vitamin B12• This relation has been
demonstrated through vitamin Bn-dependent and non-dependent Clostridium
cochlearium cells; the dependent cells were able to methylate mercury while the
non-dependent cells were not able to do so. In any case, both strains were able to
transport HgH at the same rate; however, the rate at which the different strains
were able to resist its presence was markedly different (Wood and Wang 1983).
Hughes and Poole (1989) also considered the involvement of methylcobalamin as
the primary route for the non-enzymatic methylation, also mentioning Sadenosylmethionine or 5-methyl-tetrahydrofolate as methyl donors. They also
discuss the enzymatic route through inductive systems for the conversion of
mercury compounds to volatile species; in this case, the role of mercuric
reductase in Pseudomonas spp., E. coli and S. aureus, is mentioned, all plasmidcontaining strains and organomercurial lyases, from soil Pseudomonas strain
K62. The authors discuss the mechanism of resistance involved, indicating that
there is a specific plasmid-encoded transport of HgH in the direction of the cells,
in order to prevent the reaction of the toxic element with the sulphydryl groups
present in the membranes. Once again, it is stressed that even though
metabolically mediated reactions can take place, the initial step of the
incorporation of mercury is not exactly metabolically driven.
These detoxification mechanisms are also discussed in another paper
(Summers and Silver 1978). The authors state that there are different detoxification mechanisms, as expected, indicating three different routes for HgH
detoxification in microbial cultures: (1) synthesis of mercury binding thiols; (2)
the existence of permeability barriers that could limit the access of toxic
materials against the cells; and (3) elimination of the toxic element for the culture
medium. In the detoxification of organomercurials it is proposed a mechanism
involving the degradation of the associated alkyl/aryl radical, followed by the
reduction of HgH to volatile Hgo.
In order not to restrict the discussion on bacterial cells, Overnell (1975) work,
attributed to mercury a toxic effect associated with the loss of cell potassium in
two marine algae species, Dunaliella tertiolecta and Phaeodactyium tricornutum.
The author explains that, in these algal species, mercury is probably transported
through the outer membrane of the cells to the chloroplasts, preventing
photosynthetic activity, even though no cell membrane damage has been
observed. In this work it is also mentioned that in Chiorella pyrenoidosa the
primary toxic effect of mercury is to induce leakage of the cells, thus outflowing
cell potassium.
For another green microalgae, Chlorella, the effect of sublethal concentrations
of mercury, added in its culture medium as HgCl2 , proved to affect the growth
rate. The effect on the growth rate was due to the absorption of mercury, in this
case, restricted to 14% in the cell wall (de Filippis and Pallaghy 1976).
Further, de Filippis (1978) observed that cultures of the same microalgae
Chiorella, with an inducible resistance to mercury compounds, show an
175
considerations, one can envisage that heavy metal elements present a wide range
of activity on microbial cells, some biochemical effects, being described in the
literature concerning microbial metabolism of any structural change in the cells.
Another methylation mechanism described in the literature involves the
synthesis of metal alkyls related to vitamin B12• This relation has been
demonstrated through vitamin Bn-dependent and non-dependent Clostridium
cochlearium cells; the dependent cells were able to methylate mercury while the
non-dependent cells were not able to do so. In any case, both strains were able to
transport HgH at the same rate; however, the rate at which the different strains
were able to resist its presence was markedly different (Wood and Wang 1983).
Hughes and Poole (1989) also considered the involvement of methylcobalamin as
the primary route for the non-enzymatic methylation, also mentioning Sadenosylmethionine or 5-methyl-tetrahydrofolate as methyl donors. They also
discuss the enzymatic route through inductive systems for the conversion of
mercury compounds to volatile species; in this case, the role of mercuric
reductase in Pseudomonas spp., E. coli and S. aureus, is mentioned, all plasmidcontaining strains and organomercurial lyases, from soil Pseudomonas strain
K62. The authors discuss the mechanism of resistance involved, indicating that
there is a specific plasmid-encoded transport of HgH in the direction of the cells,
in order to prevent the reaction of the toxic element with the sulphydryl groups
present in the membranes. Once again, it is stressed that even though
metabolically mediated reactions can take place, the initial step of the
incorporation of mercury is not exactly metabolically driven.
These detoxification mechanisms are also discussed in another paper
(Summers and Silver 1978). The authors state that there are different detoxification mechanisms, as expected, indicating three different routes for HgH
detoxification in microbial cultures: (1) synthesis of mercury binding thiols; (2)
the existence of permeability barriers that could limit the access of toxic
materials against the cells; and (3) elimination of the toxic element for the culture
medium. In the detoxification of organomercurials it is proposed a mechanism
involving the degradation of the associated alkyl/aryl radical, followed by the
reduction of HgH to volatile Hgo.
In order not to restrict the discussion on bacterial cells, Overnell (1975) work,
attributed to mercury a toxic effect associated with the loss of cell potassium in
two marine algae species, Dunaliella tertiolecta and Phaeodactyium tricornutum.
The author explains that, in these algal species, mercury is probably transported
through the outer membrane of the cells to the chloroplasts, preventing
photosynthetic activity, even though no cell membrane damage has been
observed. In this work it is also mentioned that in Chiorella pyrenoidosa the
primary toxic effect of mercury is to induce leakage of the cells, thus outflowing
cell potassium.
For another green microalgae, Chlorella, the effect of sublethal concentrations
of mercury, added in its culture medium as HgCl2 , proved to affect the growth
rate. The effect on the growth rate was due to the absorption of mercury, in this
case, restricted to 14% in the cell wall (de Filippis and Pallaghy 1976).
Further, de Filippis (1978) observed that cultures of the same microalgae
Chiorella, with an inducible resistance to mercury compounds, show an