Elevated Heavy Metals: A Stress on a Population of White Suckers, <i>Catostomus commersoni</i>, in Hamell Lake, Saskatchewan

McFarlane, G. A.; Franzin, William G.

doi:10.1139/f78-157

Cited by 62 publications

(28 citation statements)

References 1 publication

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“…In conclusion it seems that levels of 0.1 fiM Cd (11 parts per billion), which are close to those found in Cdpolluted freshwaters (18), disturb the fish's Ca balance by a specific effect on the branchial Ca2+ uptake mech anism. Insight in the development of hypocalcemia that seems inherent to the toxic effects of sublethal amounts of Cd2+ may be of primary importance for the under standing of Cd2+ toxicity in fish.…”

Section: Ca2+ Effluxsupporting

confidence: 55%

“…1) Cd2+ (0.01 < Cd2+ < 1.0 ^M) is able to disturb Ca2+ fluxes in the gills of trout without affecting Na balance in these fish. 2) Cd2+ (0.01 < Cd2+ < 0.1 fiM) inhibits Ca2+ influx via the gills at concentra tions close to those occurring in polluted freshwaters (18). 3) Cd2+ does not interfere with the entrance of Ca2+ across the apical membranes into the cell, but rather inhibits Ca2+ extrusion via the basolateral membrane because the tissue Ca2+ content is not reduced on Cd exposure via the water.…”

Section: Discussionmentioning

confidence: 98%

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Cadmium inhibition of Ca2+ uptake in rainbow trout gills

Verbost¹,

Flik²,

Lock³

et al. 1987

American Journal of Physiology-Regulatory, Integrative and Comp

111

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The effects of cadmium (Cd2+) on calcium (Ca2+) transport in the gills of rainbow trout (Salmo gairdneri) were studied. The gill epithelium of freshwater fish represents a model for a Ca2+-transporting tight epithelium. Unidirectional Ca2+ fluxes in the gills were estimated in an isolated saline-perfused head preparation. Ca2+ influx was not affected when up to 10 microM Cd were added to the ventilatory water at the start of flux determinations (in vitro exposure). However, after 16 h in vivo preexposure of the fish to 0.1 microM Cd in the water, a 79% inhibition of Ca2+ influx was observed. Ca2+ efflux was not affected when up to 10 microM Cd were added to the ventilatory water during the flux determination. Ca2+ efflux in fish preexposed to 0.1 microM Cd for 16 h was also not affected; a preexposure to 1 microM Cd, however, resulted in a 173% increase in Ca2+ efflux rates. Tracer retention in the gill tissue indicated that both Ca2+ and Cd2+ enter the gill epithelium via a lanthanum (La3+)-inhibitable pathway. It is concluded that Cd2+ readily enters the branchial epithelial cells, similarly as Ca2+ does via La3+-sensitive apical Ca2+ channels. The inhibitory action of Cd2+ on transepithelial Ca2+ influx seems to result from an inhibition of the basolateral Ca2+ transport, occurring after a critical intracellular Cd2+ concentration has been reached.

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Section: Ca2+ Effluxsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 98%

Cadmium inhibition of Ca2+ uptake in rainbow trout gills

Verbost¹,

Flik²,

Lock³

et al. 1987

American Journal of Physiology-Regulatory, Integrative and Comp

111

View full text Add to dashboard Cite

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“…Under toxic stress population size decreases, growth of individuals increases, more young are produced per female, the proportion of oviparious females increases substantially, and the birth rate increases. Similar factors have been observed operating in fish populations responding to exploitation (McFadden 1977,Jensen 1971 and to heavy metal toxic stress (McFarlane and Franzin 1978).…”

Section: (8)supporting

confidence: 66%

Toxicant-induced fecundity compensation: A model of population responses

Jensen

Marshall

1983

Environmental Management

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/ A mathematical model widely applied in population studies and in assessment of the impact of exploitation on fish populations was applied to assess cadmium toxicity in laboratory populations of Daphnia galeata mendotae. Over a range of toxicant concentrations, the birth rate of the population increased to balance the death rate and the population compensated for the increased mortality. The model describes the relation between toxicant concentration, toxicant-induced mortality, and equilibrium population size. Compensation for increased mortality is described in terms of the decrease in population size necessary to produce an increase in the birth rate that will balance the increased death rate. The relative capacity of different aquatic organisms to compensate for toxicant-induced mortality is examined and a relation between compensatory capacity and the innate capacity for increase is developed.Populations subjected to mortality induced by exposure to toxicants compensate to offset this mortality so that its impact on populations will not be as severe as observations of individuals indicate. Compensation provides a margin of safety, but its results are gradual and more difficult to detect. In this study a mathematical mode) is developed and applied to describe the toxic impact, of cadmium on laboratory populations of Daphnia and the responses of the populations to this impact. The model is applied to examine the relations among the levels of stress, population size, birth rate, and death rate. The ModelA mortality equation for some concentration of a toxicant that increases the death rate iswhere D is the number of toxicant-induced deaths, N is the population size, and Z is the toxicant-induced mortality rate per individual. The toxicant-induced mortality rate is a function of toxicant concentration; the simplest relation isKEY WORDS Toxicant-induced mortality; Environmental modeling; Fecundity compensation lWork performed under the auspices of the United States Environmental Protection Agency. 9 Work completed while on sabbatical leave at Argonne National Laboratory.for C --Co, where h is the toxicant-induced mortali*.yin #g/L, and Co is the threshold toxicant concentration (which might be zero).To apply the toxicant mortality equation, an equation must be developed for change in population size. The capacity of a population to compensate for increased mortality is a function of population size with the compensatory capacity low at both low and high population sizes and a maximum at some intermediate population size. Application of a parabola to describe the relation between the capacity to increase and population size, which is the simplest approach, gives the modelwhere the new symbols are r is the innate capacity for the population to increase (time) -l, and K which is the environmental carrying capacity in numbers. The above population growth equation is the logistic equation. The toxicity of a chemical under a particular set of conditions and the sensitivity of the individuals tested determines...

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“…Increased metal concentrations in the gonads likely implicate a direct burden for reproduction and/or for young fish in addition to indirect effects on regulatory systems at other sites. Studies of Eaton (1973) and McFarlane and Franzin (1978) showed that exposure to mixtures of trace metals decreased the reproductive success of fathead minnows and white suckers.…”

Section: Gonadsmentioning

confidence: 99%