Abstract

Zinc is an essential micronutrient that becomes toxic at elevated concentrations. Under hypoxic events, i.e., temporal depletion of oxygen, the toxicity of Zn increases for fish, apart from the direct effects of the reduced oxygen levels. This enhanced toxicity currently is explained by the increased ventilation rates under hypoxia, causing a higher water flow over the gills. However, the few experimental studies available on the uptake of heavy metals under hypoxia draw contradictory conclusions. The present study verifies the enhanced zinc toxicity under hypoxia and tests whether accumulation of zinc is increased in common carp, Cyprinus carpio (L.). Second, the effect of acclimatization to three oxygen levels (100, 50, and 25% saturation) on the zinc uptake and elimination was studied in a standard radiotracer uptake-and-elimination study for 63 d at 100 nmol/L Zn and 25 degrees C. The sensitivity of carp for Zn was threefold higher under hypoxia than at normoxic conditions. The lethal concentration for 50% of the population after 96 h (96-h LC50) for normoxia and hypoxia (25%) were 149 (91-317) and 55 (30-100) micromol/L Zn, respectively. However, the kinetic data indicate that zinc uptake and elimination are not altered under hypoxia for common carp. Moreover, observed uptake rates are considerably lower than predicted from a ventilation-and-diffusion-regulated uptake mechanism. Setting these results in the framework of similar experiments of other investigators, we conclude that, in general, metal uptake in fish is not related to its ventilation rate within a normal physiological range.

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