are also absorbed from seawater, then it can be assumed that the same mechanisms
are activated as for the essential two-valence trace elements. It is possible that mercury, cadmium, and lead also behave like zinc or copper during ultrafiltration from
the blood to primary urine and during reabsorption in the kidneys. To be sure, zinc
and copper are necessary, but they are also poisonous in higher concentrations. To
date, no biochemical reactions are known in which mercury, cadmium, and lead play
a positive role. For this reason, these elements, even in the smallest concentrations,
are held to be basically toxic, that is, they have a negative effect on physiological
processes. That organisms continue to survive in the sea despite this is due to the fact
that they tolerate the toxicity of these trace elements, not only at the low concentrations that occur naturally in seawater, but also in the higher concentrations which
organisms inevitably accumulate in their tissues. By and large, uptake mechanisms
cause more trace elements to be absorbed than the organism needs (Bryan 1976b).
Excretion processes see to it that trace elements are eliminated, too; if excretion is
not sufficient, toxic trace elements may be transformed into a nontoxic compound
and stored away in liver or kidney, or even in hair, feathers, or in the calcareous shell
of molluscs. As long as excretion and storage mechanisms are effective, sensitive tissues like the brain are protected from accumulating too high concentrations of toxic
elements which might be harmful to physiological processes.
In detail, physiological and biochemical strategies for uptake, storage, and elimination of toxic heavy metals may differ widely. For example, predatory fish of the
same 40-50 cm length living under very similar environmental conditions at a depth
of 2500 m have very different mercury concentrations in their flesh: Aldrovandia
macrochir a mere 0.07-0.08 mg/kg; Antimora rostrata, on the other hand, 0.50.7 mg/kg, ten times as much on wet weight basis (Barber et al. 1972). These figures
could indicate different growth rates and, therefore, different ages for fish of the
same size, or different physiological adaptations to mercury uptake.
Larger predators among marine animals absorb considerable amounts of heavy metal
through the fish they eat. Cases are well known in sharks and other large edible fish,
for example (see Chap. 8.2). Seals that absorb highly toxic methylmercury through
the fish they eat also have a long life. Seals accumulate mercury in their liver, but no
more than 15% methylmercury has been found in them. The greater part is present
in less toxic form and has apparently been detoxified. Their brain, which is sensitive
to mercury, is protected from high concentrations by the mercury's being stored up
in their liver. Only when the mercury concentration in their liver rises above 200 mg/
kg, relative to wet weight, does their protective mechanism fail. Then the brain also
attains high concentrations (Roberts et al. 1976).
In experiments with rats and quails, scientists were able to prove that selenium diminishes the toxic effect of mercury. In swordfish and seals, the concentration of selenium increases with that of the mercury (Table 33 and Fig. 72). According to findings in California sea lions (Zalophus cali[ornilmus), there are indications that the
proportion of the atom equivalents of mercury, selenium, and bromine, not the absolute quantities plays a role; stillbirths are more common if the proportion is not 1: 1: 1
(Martin et al. 1976). In the connective tissue of the liver of dolphins, concentrations
of pure mercury selenide were found, apparently a product of detoxification of the
methylmercury absorbed through their diet of fish (Martoja and Viale 1977).
135
are activated as for the essential two-valence trace elements. It is possible that mercury, cadmium, and lead also behave like zinc or copper during ultrafiltration from
the blood to primary urine and during reabsorption in the kidneys. To be sure, zinc
and copper are necessary, but they are also poisonous in higher concentrations. To
date, no biochemical reactions are known in which mercury, cadmium, and lead play
a positive role. For this reason, these elements, even in the smallest concentrations,
are held to be basically toxic, that is, they have a negative effect on physiological
processes. That organisms continue to survive in the sea despite this is due to the fact
that they tolerate the toxicity of these trace elements, not only at the low concentrations that occur naturally in seawater, but also in the higher concentrations which
organisms inevitably accumulate in their tissues. By and large, uptake mechanisms
cause more trace elements to be absorbed than the organism needs (Bryan 1976b).
Excretion processes see to it that trace elements are eliminated, too; if excretion is
not sufficient, toxic trace elements may be transformed into a nontoxic compound
and stored away in liver or kidney, or even in hair, feathers, or in the calcareous shell
of molluscs. As long as excretion and storage mechanisms are effective, sensitive tissues like the brain are protected from accumulating too high concentrations of toxic
elements which might be harmful to physiological processes.
In detail, physiological and biochemical strategies for uptake, storage, and elimination of toxic heavy metals may differ widely. For example, predatory fish of the
same 40-50 cm length living under very similar environmental conditions at a depth
of 2500 m have very different mercury concentrations in their flesh: Aldrovandia
macrochir a mere 0.07-0.08 mg/kg; Antimora rostrata, on the other hand, 0.50.7 mg/kg, ten times as much on wet weight basis (Barber et al. 1972). These figures
could indicate different growth rates and, therefore, different ages for fish of the
same size, or different physiological adaptations to mercury uptake.
Larger predators among marine animals absorb considerable amounts of heavy metal
through the fish they eat. Cases are well known in sharks and other large edible fish,
for example (see Chap. 8.2). Seals that absorb highly toxic methylmercury through
the fish they eat also have a long life. Seals accumulate mercury in their liver, but no
more than 15% methylmercury has been found in them. The greater part is present
in less toxic form and has apparently been detoxified. Their brain, which is sensitive
to mercury, is protected from high concentrations by the mercury's being stored up
in their liver. Only when the mercury concentration in their liver rises above 200 mg/
kg, relative to wet weight, does their protective mechanism fail. Then the brain also
attains high concentrations (Roberts et al. 1976).
In experiments with rats and quails, scientists were able to prove that selenium diminishes the toxic effect of mercury. In swordfish and seals, the concentration of selenium increases with that of the mercury (Table 33 and Fig. 72). According to findings in California sea lions (Zalophus cali[ornilmus), there are indications that the
proportion of the atom equivalents of mercury, selenium, and bromine, not the absolute quantities plays a role; stillbirths are more common if the proportion is not 1: 1: 1
(Martin et al. 1976). In the connective tissue of the liver of dolphins, concentrations
of pure mercury selenide were found, apparently a product of detoxification of the
methylmercury absorbed through their diet of fish (Martoja and Viale 1977).
135