Acute Toxicity of Some Heavy Metals to<i>Lates</i><i>calcarifer</i>Fry with a Note on Its Histopathological Manifestations

Krishnani, Kishore Kumar; Azad, I.S.; Kailasam, M.; Thirunavukkarasu, A. R.; Gupta, B. P.; Joseph, K. O.; Muralidhar, M.; Abraham, Mathew

doi:10.1081/ese-120016929

Cited by 38 publications

(18 citation statements)

References 10 publications

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“…In contrast to embryo studies, significantly more work has been reported on the histopathology of mercury in older fish (Hammerschmidt et al, 2002;Ribeiro et al, 2002;Drevnick and Sandheirich, 2003;Krishnani et al, 2003). Several of the histopathological effects of MeHg on the fathead minnow reported in the current study have also been noted by the author in embryos of the coho salmon and rainbow trout Mottet, 1991, 1992).…”

Section: Embryo Pathologysupporting

confidence: 47%

Acute Toxicity, Uptake and Histopathology of Aqueous Methyl Mercury to Fathead Minnow Embryos

Devlin

2006

Ecotoxicology

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Early life stages of fishes have been shown to be especially susceptible to the toxic effects of heavy metal pollution. In this study, fathead minnow (Pimephales promelas) embryos were exposed in the laboratory to a graded series of aqueous methyl mercury concentrations under continuous-flow conditions. A number of toxicological endpoints were examined including; acute toxicity, bioaccumulation, protein production, impact on mitosis, gross and histopathology. Acute toxicity, reported as LC50 values of methyl mercury, ranged from 221 microg/l (95% C.I. 246-196 microg/l) for 24-h tests to 39 microg/l (95% C.I. 54-24 microg/l) for 96-h exposures. Fathead minnow embryos were shown to rapidly take up mercury from the surrounding water. Mercury levels in embryos reached levels of 2.80 microg/g wet weight after 96 h exposure to 40 microg/l methyl mercury. An initial elevation of total protein in embryo was observed in embryos exposed to 25 microg/l methyl mercury during the first 12 h of development. At later stages, significantly lower levels of protein/microg embryo were observed. Methyl mercury had no effect on mitotic stages (p=0.05) in early, cleaving blastula-stage embryos. Live embryos and serial sections were utilized to characterize changes in embryo morphology and histopathology.

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Section: Embryo Pathologysupporting

confidence: 47%

Acute Toxicity, Uptake and Histopathology of Aqueous Methyl Mercury to Fathead Minnow Embryos

Devlin

2006

Ecotoxicology

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“…In euryhaline killifish Fundulus heteroclitus (96-h LC50: 18 mg Cu/L in freshwater and 294 mg Cu/L in 35% seawater) and topsmelt Atherinops affinis (168-h LC50: 44, 72, 134, and 205 mg Cu/L in 10, 17, 25, and 34% waters, respectively), larvae also became less sensitive to Cu as salinity increased [22,23]. In the present study, the 96-h LC50 for red sea bream larvae was 0.13 mg Cu/L, which falls within the reported values for other marine fish larvae [10,[19][20][21]. Copper toxicity in fish at ELS is substantially affected by salinity.…”

Section: Acute Toxicity Of Coppersupporting

confidence: 83%

“…Under similar experimental conditions, the 96-h LC50 values of Cu for a large majority of the reported freshwater fish larvae varied remarkably from 3.4 mg Cu/L for Chinook salmon to 690 mg Cu/L for blue tilapia Oreochromis aureus [17,18]. In the few tested marine fish larvae, these values ranged from 68 mg Cu/L for anchovy Engraulis japonicus to 1,800 mg Cu/L for sea bass Lates calcarifer [10,[19][20][21]. These results suggest that marine fish larvae might tolerate Cu exposure more than their freshwater counterparts.…”

Section: Acute Toxicity Of Coppermentioning

confidence: 87%

Toxicity of short‐term copper exposure to early life stages of red sea bream, Pagrus major

Cao

Huang

Lü

et al. 2010

Enviro Toxic and Chemistry

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Acute (0, 0.1, 0.2, 0.4, 0.8, 1.6 mg Cu/L) and chronic (0, 0.02, 0.04, 0.06, 0.08, 0.10, 0.12 mg Cu/L) toxicity tests of Cu with embryonic and larval red sea bream, Pagrus major, were carried out to investigate their biological responses to Cu exposure in static water at 18 +/- 1 degrees C (dissolved organic carbon, 1.8 +/- 0.65 mg C/L; hardness, 6,183 +/- 360 mg CaCO3/L; salinity, 33 +/- 1 per thousand). The 24- and 48-h LC50 (median lethal concentration) values of Cu for embryos were 0.23 and 0.15 mg/L, whereas the 48-, 72-, and 96-h LC50 values for larvae were 0.52, 0.19, and 0.13 mg/L, respectively, suggesting that embryos were more sensitive to Cu toxicity than larvae. Copper exposures at > or =0.06 mg concentrations caused low hatching success, a delay in the time to hatching of embryos, and reductions in the growth and yolk absorption of the larvae, whereas high mortality and morphological malformations occurred in the embryos and larvae at > or =0.08 mg/L concentrations. Copper concentration did not significantly affect the heart rate of the embryos, but it significantly decreased the heart rate of the newly hatched larvae when the Cu concentration was > or =0.08 mg/L, suggesting that Cu at high concentrations could induce heartbeat disturbances in red sea bream more easily at the larval stage than at the embryonic stage. Hatching success, time to hatching, growth rate, morphological abnormality, yolk absorption, and heart rate were Cu concentration-dependent and could be effective endpoints for evaluating Cu toxicity to the early life stages of red sea bream in nature.

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“…Experimental studies on heavy metals proved that they could impair the respiratory functions of the gills; consequently death in fish is probably caused by tissue hypoxia [11]. Metals affect not only the fish morphology, but also all biological activities [12]. Among the heavy metals; Cd and Pb are the serious heavy metals that produce histopathological alterations including liver damage [13], respiratory dysfunctions [14], testicular and ovarian alterations [15][16][17].…”

Section: Introductionmentioning

confidence: 99%

Impact of Environmental Contaminants on the Testes of Oreochromis niloticus with Special Reference to Ultrastructure of Spermatozoa in Lake Manzala (Egypt)

Shalaby¹,

Migeed²

2012

J Environ Anal Toxicol

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IntroductionThe importance of Nile tilapia, Oreochromis niloticus in aqua cultures is due to its spreading in most countries of the world [1]. It breads in captivity and wide variety of water conditions [2]. Lake Manzalah (LM) is one of the most important lakes in Egypt that provides more than 70% of the total fishery of the country [3] and considered as a highly polluted with toxic heavy metals and pesticides due to progressive increase of industrial and agricultural drainage, as well as sewage out fall from the surrounding governorates [4]. The mean values of some heavy metals (Cd, Pb, Fe, Cr and Mn) recorded in LM were higher than the world permissible levels [5] and according to the Egyptian laws [6]. Such heavy metals are not lethal to fish, but concentrated in their flesh and create a hazard to the consumer [7,8]. Cd, Pb, Zn, and Cr are considered the main causes of pollution in aquatic ecosystem [9]. The serious effect of these metals is derived from their persistence, toxicity and bioaccumulation, and consequently exert dangerous problem to man [10]. Experimental studies on heavy metals proved that they could impair the respiratory functions of the gills; consequently death in fish is probably caused by tissue hypoxia [11]. Metals affect not only the fish morphology, but also all biological activities [12]. Among the heavy metals; Cd and Pb are the serious heavy metals that produce histopathological alterations including liver damage [13], respiratory dysfunctions [14], testicular and ovarian alterations [15][16][17]. These pathological alterations were primarily attributed to damage of cell membranes which allows higher uptake of Cd and Pb and thus the injury extends to more critical targets [18]. Many studies focused on bioaccumulation of heavy metals in fish and biological studies. Thus we aimed in this work to study the testicular histopathological alterations of Oreochromis niloticus using light microscope and the mature sperm using TEM. Materials and Methods Samples collectionSamples of water and 48 specimen of Nile tilapia, Oreochromis niloticus about 14-20 cm in length and 120-200 g in weight were collected from two areas; Demitta branch of RN at Mansoura city as a control site and LM as a polluted area during the spawning season from March-June and transported to the laboratory in tanks provided with oxygen pump. The fish were weighed, dissected and the testes were Abstract Background: Pollution of the aquatic environment by inorganic and organic chemicals is a major factor posing serious threat to the survival of aquatic organisms including fish. Lake Manzala (LM) is one of the Egypt's northern Delta Lakes situated on the Mediterranean Coast of the Delta. It is affected by drainage water polluted by different heavy metals that their concentrations exceed the maximum world permissible levels.

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Acute Toxicity of Some Heavy Metals toLatescalcariferFry with a Note on Its Histopathological Manifestations

Cited by 38 publications

References 10 publications

Acute Toxicity, Uptake and Histopathology of Aqueous Methyl Mercury to Fathead Minnow Embryos

Acute Toxicity, Uptake and Histopathology of Aqueous Methyl Mercury to Fathead Minnow Embryos

Toxicity of short‐term copper exposure to early life stages of red sea bream, Pagrus major

Impact of Environmental Contaminants on the Testes of Oreochromis niloticus with Special Reference to Ultrastructure of Spermatozoa in Lake Manzala (Egypt)

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