Abstract:This study documents the successful use of a mysid, Mysidopsis bahia, for life-cycle toxicity tests. These tests were conducted to determine acute and chronic toxicities of metal (cadmium) and pesticide (Kepone). Delay in the formation of mysid brood pouches and release of young were noted in low concentrations ⩽6.4μg cadmium/litre. Fewer young produced per female and decreased growth were other indicators of effects of Kepone.
“…We do not know why R. harrisii larvae are so much more resistant to Kepone than to mirex. The range of concentrations of Kepone in which development of the decapod, C. sapidus, occurred (Table V) was much more narrow than the range reported for the survival of 48-h-old juvenile Mysidopsis bahia, a mysid, exposed to different concentrations of Kepone for 19 days (Nimmo et aL, 1977). Survival of mysids was 90.6% in pg l-~, 84.4% in 0.39/Jg 1-~, 50% in 1.55 Pg 1-~, 3.1% in 4.4 pg l-1 and 0% in 8.7 pg 1-~.…”
Section: Survivalmentioning
confidence: 82%
“…Kepone is readily taken from water by marine organisms (Waish et al, 1977;Schimmel and Wilson, 1977;Nimmo et aL, 1977;Hansen et aL, 1977b), and is passed through a food chain . Depuration varies among species tested.…”
Section: Introductionmentioning
confidence: 99%
“…Hansen et aL (1977a) studied the chronic effects of Kepone on embryo, fry, juvenile and adult sheepshead minnows (Cyprinodon variegatus). The only life history toxicity tests on a malacostracan crustacean have been made on mysids, Mysidopsis bahia (Nimmo et aL, 1977).…”
Abstract. Laboratory experiments were conducted to determine the effects of Kepone on the larval development of the mud-crab, Rhithropanopeus harrisii, and the commercial blue crab, Callinectes sapidus, from the time of hatching until the 1 st crab stage was reached.Differential survival of R. harrisii from hatching to 1st crab stage occurred in a range of 35 to 125 ppb Kepone, whereas differential survival of C. sapidus over the same period of development occurred in a range of 0.1 to 1.0 ppb. Statistical analysis indicated that, for every 10 ppb Kepone added, duration from hatching to 1st crab stage of R. harrisii was increased by 0.391 + 0.043 days; whereas for each increase of 0.1 ppb, the duration from hatching to 1st crab stage of C. sapidus is prolonged by 0.38 + 0.10 days. The 1st and 2nd zoeal stages of R. harris# were the most sensitive developmental stages to Kepone, but the 1st zoeal stage of C. sapidus was not sensitive, statistically, to any concentration of Kepone tested. In zoeal stages II, IIl and IV, there were significant increases in mortality of C. sapidus over the previous stage in all media tested.
“…We do not know why R. harrisii larvae are so much more resistant to Kepone than to mirex. The range of concentrations of Kepone in which development of the decapod, C. sapidus, occurred (Table V) was much more narrow than the range reported for the survival of 48-h-old juvenile Mysidopsis bahia, a mysid, exposed to different concentrations of Kepone for 19 days (Nimmo et aL, 1977). Survival of mysids was 90.6% in pg l-~, 84.4% in 0.39/Jg 1-~, 50% in 1.55 Pg 1-~, 3.1% in 4.4 pg l-1 and 0% in 8.7 pg 1-~.…”
Section: Survivalmentioning
confidence: 82%
“…Kepone is readily taken from water by marine organisms (Waish et al, 1977;Schimmel and Wilson, 1977;Nimmo et aL, 1977;Hansen et aL, 1977b), and is passed through a food chain . Depuration varies among species tested.…”
Section: Introductionmentioning
confidence: 99%
“…Hansen et aL (1977a) studied the chronic effects of Kepone on embryo, fry, juvenile and adult sheepshead minnows (Cyprinodon variegatus). The only life history toxicity tests on a malacostracan crustacean have been made on mysids, Mysidopsis bahia (Nimmo et aL, 1977).…”
Abstract. Laboratory experiments were conducted to determine the effects of Kepone on the larval development of the mud-crab, Rhithropanopeus harrisii, and the commercial blue crab, Callinectes sapidus, from the time of hatching until the 1 st crab stage was reached.Differential survival of R. harrisii from hatching to 1st crab stage occurred in a range of 35 to 125 ppb Kepone, whereas differential survival of C. sapidus over the same period of development occurred in a range of 0.1 to 1.0 ppb. Statistical analysis indicated that, for every 10 ppb Kepone added, duration from hatching to 1st crab stage of R. harrisii was increased by 0.391 + 0.043 days; whereas for each increase of 0.1 ppb, the duration from hatching to 1st crab stage of C. sapidus is prolonged by 0.38 + 0.10 days. The 1st and 2nd zoeal stages of R. harris# were the most sensitive developmental stages to Kepone, but the 1st zoeal stage of C. sapidus was not sensitive, statistically, to any concentration of Kepone tested. In zoeal stages II, IIl and IV, there were significant increases in mortality of C. sapidus over the previous stage in all media tested.
The epibenthic mysid Mysidopsis bahia was chronically exposed throughout its entire life cycle to inorganic mercury. The experimental design permitted the precise measurements of survival rates; individual and population growth rates; and sublethal reproductive responses, including time to sexual maturation and first brood release, egg development time, brood size and frequency of reproduction. Mercury was acutely toxic (96‐h LC50) to juveniles at 3.5 μg L−1, chronically toxic (35‐d LC50) at 1.8 μg L−1 and differentially toxic to males and females (α = 0.05). Male and female mortality rates were 35 and 18%, respectively, from sexual maturation (day 14) through termination of the assay (day 35). Reproductive effects included delays in sexual maturation and brood release at 1.6 μg L−1, a doubling of brood development time at 2.5 μg L−1 and subsequent abortion and significant decreases in the total broods released (and therefore juveniles produced) at 1.6 μg L−1. Intrinsic rates of population increase (r), calculated from life‐tables, decreased with increasing mercury concentration. The critical value (r = 0) for mercury occurs at 1.6 μg L−1, which corresponds well with the upper limit of the maximum acceptable toxicant concentration, the usual endpoint of life‐cycle toxicity tests. The toxicity test system is a sensitive, precise model for studying lethal, sublethal and potential population consequences of pollution.
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