Subacute intoxication of a deltamethrin-based preparation (Butox) 5% EC) in monosex Nile tilapia, Oreochromis niloticus L

The monosex Nile tilapia, Oreochromis niloticus L., was exposed to subacute concentration (1.46 microg/l) of a pyrethroid insecticide, deltamethrin for 28 consecutive days. Behavioural, clinical, haematological, serum biochemical and histopathological consequences were assayed at a regular interval of 7 days. The abnormal behavioural responses and toxic symptoms were described. Exposure to deltamethrin not only significantly decreased lymphocyte and basophile percentages, total leucocytic and total erythrocytic counts, haemoglobin percentage and packed cell volume value, but also caused serious effects in the form of hypoproteinaemia, hypoalbuminaemia, hypercholesterolaemia, hyperglycaemia and significantly increased serum aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase activities. Moreover, the histopathological results indicated that the haemobiotic organs were affected by deltamethrin, primarily liver and gills. Our data suggest that subacute exposure to deltamethrin exerts a serious metabolic distress on the fish corresponding to the exposure period. In addition, the assayed parameters and histopathological findings can be as good biomarkers of pyrethroid ecosystem pollution.     

Acute intoxication of deltamethrin in monosex Nile tilapia, Oreochromis niloticus with special reference to the clinical, biochemical and haematological effects

Deltamethrin, a synthetic pyrethroid pesticide, potential toxic pollutant and significant direct risk to the aquatic ecosystems, was investigated in the present study for its toxic impact on adult monosex Nile tilapia on the basis of acute static bioassay test, and comparison of clinical, biochemical and haemato logical examinations with deltamethrin-free control group. The 96 hLC₅₀ value of deltamethrin for monosex tilapia was 14.6 μg/L. The abnormal behavioral responses and toxic symptoms were described. Fish exposed to the higher deltamethrin concentration (15 μg/L) for 96 h showed significantly higher lymphocytes, total leucocytic and erythrocytic counts, haemoglobin percentage and packed cell volume content and significantly lower neutrophils compared to the control group. Deltamethrin caused adverse effects in the form of hypoproteinemia, hypoalbuminemia, hypercholesterolemia, hypoglycemia and significant increase of serum aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase activities. The results provide evidence that deltamethrin pollution may have adverse impacts and was highly toxic to monosex tilapia.     

Acute intoxication of deltamethrin in monosex Nile tilapia,Oreochromis niloticus with special reference to the clinical,biochemical and haematological effects

Deltamethrin, a synthetic pyrethroid pesticide, potential toxic pollutant and significant direct risk to the aquatic ecosystems, was investigated in the present study for its toxic impact on adult monosex Nile tilapia on the basis of acute static bioassay test, and comparison of clinical, biochemical and haemato logical examinations with deltamethrin-free control group. The 96 hLC₅₀ value of deltamethrin for monosex tilapia was 14.6 μg/L. The abnormal behavioral responses and toxic symptoms were described. Fish exposed to the higher deltamethrin concentration (15 μg/L) for 96 h showed significantly higher lymphocytes, total leucocytic and erythrocytic counts, haemoglobin percentage and packed cell volume content and significantly lower neutrophils compared to the control group. Deltamethrin caused adverse effects in the form of hypoproteinemia, hypoalbuminemia, hypercholesterolemia, hypoglycemia and significant increase of serum aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase activities. The results provide evidence that deltamethrin pollution may have adverse impacts and was highly toxic to monosex tilapia.     

Physiological and oxidative stress biomarkers in the freshwater monosex Nile tilapia,Oreochromis niloticus L., exposed to pendimethalin‐based herbicide

Fish are relatively sensitive to changes in their surrounding environment, including increasing pollution. Therefore, the present study was undertaken to evaluate the impact of contamination with the pendimethalin‐based herbicide; Stomp^® 50% EC (50% pendimethalin as emulsive concentrate) on adults of the monosex Nile tilapia Oreochromis niloticus L. A total of 260 fish with body weights of 90 ± 5.0 g were used in the determination of the 96‐h LC₅₀ value and of the impacts of acute exposure to pendimethalin on physiological parameters, and oxidative stress and antioxidant biomarkers. The 96‐h median lethal concentration (96‐h LC₅₀) value of pendimethalin for monosex Nile tilapia was determined as 4.92 mg/L. Abnormal behavioral responses of the fish and the toxic symptoms of pendimethalin exposure are described. Acute exposure to pendimethalin induced leukocytosis, hyperglobulinemia, and hyperglycemia, but resulted in nonsignificant changes in other hemato‐biochemical parameters. Moreover, pendimethalin increased lipid peroxidation (LPO) and decreased levels of reduced glutathione and antioxidant enzymes; superoxide dismutase, catalase, and glutathione reductase in both liver and gill tissues, in a time‐dependent manner, with maximum alterations observed in the gills rather than the liver. We conclude that although pendimethalin is moderately toxic, it does not cause hepatorenal toxicity. However, this herbicide pollutant induces major disturbances to the antioxidant system; induction of oxidative stress and LPO is the proposed toxicodynamic pathway for such stress. © 2013 Wiley Periodicals, Inc. Environ Toxicol 30: 430–438, 2015.     

A dose-based modeling approach for accumulation and toxicity of arsenic in tilapia Oreochromis mossambicus

We proposed an approach to relate metal toxicity to the concentrations of arsenic (As) in specific target organs of tilapia Oreochromis mossambicus. The relationships among As exposure, uptake, accumulation, and toxicity of tilapia were investigated using kinetic and dynamic modeling. The biouptake rate of waterborne As through the gills of fish was dependent on exposure concentrations, in that the relationship was well described by incorporating Michaelis-Menten type uptake kinetics. The fitted bioaffinity parameter and limiting uptake flux were 3.07 +/- 2.21 microg/mL(-1) (mean +/- SD) and 2.17 +/- 0.38 microg/mL(-1)/d(-1), respectively, suggesting that a low As binding affinity of tilapia gills, yet a relatively high binding capacity was obtained. The toxicity of As was analyzed by determining the lethal exposure concentration associated with a mortality of 50% (LC50) at different integration times. Our results demonstrate that 96-h and incipient LC50s for tilapia are 28.68 (95% CI: 15.98-47.38) and 25.55 microg/mL(-1), respectively. The organ-specific internal residue associated with 50% mortality was estimated by combining the model-predicted toxicokinetic parameters and the area-under-curve (AUC)-based time-integrated concentration toxicity model. A physiologically based toxicokinetic model was constructed to elucidate the principle mechanisms that account for the observed data and to predict the kinetics of As in tilapia under different water exposure scenarios. We employed the Hill equation model to predict the organ-specific dose-response relationships. We used the liver as a surrogate of target sites to assess the As toxicity to tilapia because of its higher sensitivity to As toxic effects. The predicted mortalities never reach 50% when the tilapia were exposed to waterborne As <2 microg/mL(-1). The predicted mortality is, however, slightly higher than the observed values before the 10th day in that the profile reached the 70% maximum mortality, which is comparable to the observed data when the tilapia were exposed to 4 microg/mL(-1). Our results show that a dose-based toxicokinetic and toxicodynamic modeling approach successfully links metal exposure to bioavailability, bioaccumulation, and toxicity, under variable exposure scenarios.     

Acute toxicity impacts of hexavalent chromium on behavior and histopathology of gill, kidney and liver of the freshwater fish, Channa punctatus (Bloch)

Alteration in behavioral patterns and histopathology of gill, kidney and liver were studied in Channa punctatus, after acute exposure to hexavalent chromium. The 96h LC(50) of chromium salt, potassium dichromate was determined to be 41.75mg/L. The exposed fish displayed erratic swimming and became lethargic. The changes in gills were characterized by epithelial hyperplasia, lamellar fusion, oedema, epithelial lifting, epithelial necrosis and desquamation, aneurism as well as curling of secondary lamellae. Hypertrophy of epithelial cells of renal tubules with reduced lumens, atrophy of the renal tubules, glomeruli contraction in the Bowman's capsules and necrosis of haematopoietic tissues were observed in the trunk kidney of exposed fish. The interrenal cells of the head kidney exhibited distinct hypertrophy and vacuolization. The liver hepatocytes showed cytoplasmic vacuolization with the lateral nuclei arrangement. Hepatocytes atrophy and increase in sinusoidal space were also observed. The result showed that acute chromium toxicity severely affects the vital organs and normal behavior which may be deleterious for fish populations.     

Cadmium tolerance in the Nile tilapia (Oreochromis niloticus) following acute exposure: assessment of some ionoregulatory parameters

The Nile tilapia (Oreochromis niloticus) can tolerate very high levels of waterborne cadmium. It has one of the highest 96 h LC50 recorded for a freshwater teleost fish (14.8 mg/L Cd; hardness 50 mg/L CaCO(3)). Cadmium is known to perturb ion balance in teleost fishes. However, in an acute time course experiment, plasma Na(+) concentrations were unaffected, and plasma Ca(2+) values only decreased after 96 h exposure in a dose-independent manner. Branchial Na(+)/K(+)-ATPase activity and alpha-subunit protein level expression in crude gill homogenates were not affected by Cd exposure during this period. Branchial chloride cell numbers, identified as Na(+)/K(+)-ATPase immunoreactive cells using immunohistochemistry, decreased 24 h after exposure but recovered thereafter. Histopathological changes did not follow a consistent pattern of variation with exposure time, and the alterations noted in gill epithelium were basically nonspecific to cadmium. Because of its tolerance, it can be concluded that the tilapia O. niloticus would not be a suitable test organism to evaluate sublethal toxicity of cadmium and the realistic impact of this pollutant in the environment. However, it certainly could contribute significantly to our understanding of the toxic mechanism of cadmium exposure in aquatic organisms. This is the first work to investigate the effect of waterborne pollutants on Na(+)/K(+)-ATPase alpha-subunit protein expression in fish gills.     

Investigation of acute toxicity of cyfluthrin on tilapia fry (Oreochromis niloticus L. 1758)

Cyfluthrin, a synthetic pyrethroid pesticide contaminating aquatic ecosystems as a potential toxic pollutant, was investigated in the present study for acute toxicity. Tilapia fry (Oreochromis niloticus L. 1758) was selected for the bioassay experiments. The 48 and 72h LC(50) was determined for the tilapia fry. The experiments were repeated three times. The static test method of acute toxicity test was used. In addition, behavioral changes at each cyfluthrin concentration were determined for the individuals. Data obtained from the cyfluthrin acute toxicity tests were evaluated using the Probit Analysis Statistical Method. The 48 and 72h LC(50) value for tilapia fry were estimated as 25.82μg/L (95% confidence limits: 20.92-43.26) and 21.07μg/L (95% confidence limits: 16.21-30.39), respectively.     

Protective role of dietary Spirulina platensis against diazinon-induced Oxidative damage in Nile tilapia; Oreochromis niloticus

The current study was performed to investigate the ameliorating effect of dietary supplementation of 0.5 and 1% Spiurolina platensis (SP) diet against the sub-acute toxicity of diazinon (DZN) 0.28 mg/L in Nile tilapia. At the end of experiment after 28 days, hepatic and renal damage markers (aspartate transaminase, alanine transaminase, alkaline phosphatase, urea, uric acid and creatinine), serum biochemical parameters (total proteins, albumin, cholesterol and glucose) and tissue antioxidant status (superoxide dismutase, catalase, glutathione peroxidase, reduced glutathione and malondialdehyde) were detesrmined. The results of the current study revealed significant improvement in hepatic and renal damage markers after SP supplementation in fish exposed to DZN toxicity. Moreover, SP improved serum biochemical markers through increasing serum albumin and globulins with a significant decrease in serum glucose and cholesterol. In addition, liver, kidneys and gills antioxidant status showed a significant improvement after SP supplemented to fish exposed to DZN where a significant increase in tissue antioxidant activity were observed with a significant decline in lipid peroxidation levels. It can be concluded that, SP supplementation attenuated the toxic effect of DZN toxicity in Nile tilapia through improving liver and kidney functions with a significant enhancement of tissue antioxidant status.     

Genotoxic and oxidative stress-inducing effects of deltamethrin in the erythrocytes of a freshwater biomarker fish species, Channa punctata Bloch

Deltamethrin, an alpha-cyano class of pyrethroid insecticide is used in insect pest control and antimalaria programs in several countries including India. Although various toxic manifestations of deltamethrin are reported in mammals, its ecotoxicologic dimensions are not adequately researched in ecologically and commercially important fishes. In this study, we report genotoxic effect of deltamethrin in a biomarker fish Channa punctata (Bloch). Adult fish were exposed to three concentrations of technical grade deltamethrin (0.4, 0.8, and 1.2 microg/L) for 48 and 72 h. Ethyl methane sulfonate was used as a positive control. Fish were analyzed for induction of micronucleus (MN), nuclear abnormalities (NAs), and oxidative stress biomarkers in erythrocytes. Deltamethrin significantly induced MN and NAs accompanied by increased lipid peroxidation. Activity of antioxidant enzyme superoxide dismutase was significantly decreased but an increase was observed in reduced glutathione level after 72 h of exposure. The NAs in exposed fish included blebbed, lobed and notched nuclei, and binucleated erythrocytes. Our findings suggest that oxidative stress may, in part, be contributing to deltamethrin-induced genotoxic damage to erythrocytes. Although MN induction is a nonspecific biomarker, it may provide an indication of pollution load of deltamethrin in the affected fish population when used as part of suite of other biomarkers.     

Acid and alkaline phosphatase activities and pathological changes induced in Tilapia fish (Oreochromis sp.) exposed subchronically to microcystins from toxic cyanobacterial blooms under laboratory conditions.

The effects of microcystins (MCs) from cyanobacterial cells on the enzymatic activities of acid and alkaline phosphatases (ACP and ALP) from liver, kidney and gill tissues, and the histopathological changes in freshwater Tilapia fish (Oreochromis sp.) were investigated under laboratory conditions. Fish were exposed to cyanobacterial cells (60.0 microg MC-LR/fish per day) through their diet at different exposure times (14 and 21 days). The cells were fed to the fish in two types of oral administration: mixed with a commercial fish food or crushed into a commercial fish food so that the toxins were released. ACP and ALP activities changed in response to MCs in a time-dependent manner, and these changes were more prominent in liver and kidney. The way the MCs were administered had no influence on the biochemical parameters. Similarly, the most severe histopathological changes were observed in the same two organs, although the gills and intestines were also affected. The parenchymal architecture of the liver was dissolved, and round hepatocytes with the appearance of pyknotic nuclei were detected. Kidney lesions consisted of the dilation of Bowman's space and necrotic epithelial cells with pyknotic nuclei in the tubules. These findings suggest that low and repeated doses of MC-LR from cyanobacterial cells induce toxicity in tilapia fish although no adverse effects were detected.     

Histopathological and genotoxic effects of pollution on Nile Tilapia (Oreochromis niloticus,Linnaeus, 1758) in the Billings Reservoir (Brazil)

The Billings Reservoir shows eutrophic waters due to the large amount of sewage, and consequently, the fish can be a problem for public health. Thus, this project aimed to analyze the histological gills and liver of Nile tilapia to verify morphological changes caused by environment, and the frequency of micronuclei was done, to observe the response to genotoxic activity. We observed histological alterations in gills and livers of Nile Tilapia classified as mild to severe, and the presence of micronucleus. The results enable better environmental monitoring and quality control of this species.     

Dietary l‐carnitine prevents histopathological changes in tilapia (Oreochromis Niloticus) exposed to cylindrospermopsin

Cylindrospermopsin (CYN) is a cytotoxin highly water‐soluble, which is easily taken up by several aquatic organisms. CYN acts as a potent protein and glutathione synthesis inhibitor, as well as inducing genotoxicity, oxidative stress, and histopathological alterations. This is the first study reporting the protective effect of a l ‐carnitine (LC) pretreatment (400 or 880 mg LC/kg bw fish/day, for 21 days) on the histopathological alterations induced by pure CYN or Aphanizomenon ovalisporum lyophilized cells (400 µg CYN/kg bw fish) in liver, kidney, heart, intestines, and gills of tilapia (Oreochromis niloticus) acutely exposed to the toxin by oral route. The main histopathological changes induced by CYN were disorganized parenchyma with presence of glycogen and lipids in the cytoplasm (liver), glomerulonephritis, glomerular atrophy, and dilatation of Bowman's capsule (kidney), myofibrolysis, loss of myofibrils, with edema and hemorrhage (heart), intestinal villi with necrotic enterocytes and partial loss of microvilli (gastrointestinal tract), and hyperemia and hemorrhage (gills). LC pretreatment was able to totally prevent those CYN‐induced alterations from 400 mg LC/kg bw fish/day in almost all organs, except in the heart, where 880 mg LC/kg bw fish/day were needed. In addition, the morphometric study indicated that LC managed to recover totally the affectation in the cross sections of the proximal and distal convoluted tubules in CYN‐exposed fish. © 2015 Wiley Periodicals, Inc. Environ Toxicol 32: 241–254, 2017.     

Toxicity of copper in butterfish (Poronotus triacanthus): tissues accumulation and ultrastructural changes

The present study investigated the accumulation of copper in various tissues and ultrastructural alterations in butterfish, Poronotus triacanthus. In acute toxicity test, butterfish were exposed to 250 microg/L copper for 24 h. In subacute toxicity test, fish were exposed to 25 microg/L copper for 7 days and then returned to normal water for 48 h. The levels of copper accumulation in the tissues were determined by using an atomic absorption spectrometer. After the 7 day exposure, the highest level of copper was found in the liver, followed by kidney, gills, and muscle tissues (3.64, 0.62, 0.59, and 0.34 microg/L, respectively). The recovery group has shown some reduction in copper level in these tissues when compared with those of the 7 day exposure group (3.09, 0.34, 0.30, and 0.27 microg/L, respectively). In gills, the major changes such as filament cell proliferation, increase in intercellular spaces, epithelial lifting, and thickening of the filament and lamellar epithelium were observed. In liver, the major changes such as swollen mitochondria, fragmented in rough endoplasmic reticulum, increases in number and size of lysosomes and lipid droplets. Infiltration of leukocytes, increasing hepatocyte size with pyknotic nuclei, and presence of vacuoles were also observed. In kidney, the changes included alterations of the first proximal tubules, as well as vacuolization of the cytoplasm, proliferation of lysosomes and mitochondria, dilation of endoplasmic reticulum, and finally, cell necrosis. The transmission electron microscopic analysis revealed that the 7 day exposure group had more severe effect in tissue alterations than the 24 h exposure group. Tissue regeneration was also observed in the 48 h recovery group.     

Acute exposure of a glyphosate-based herbicide affects the gills and liver of the Neotropical fish, Piaractus mesopotamicus

The aim of this study was to determine the acute toxicity of Roundup(?) Ready (RR) in Piaractus mesopotamicus, and evaluate the effects on the morphology of the gills and liver of exposed surviving fish. Fish were exposed to 3.0, 3.5, 4.0 and 4.5mgL(-1) of glyphosate, and the LC(50);48h was estimated at 3.74±0.2mgL(-1). Gill histopathology was rare, and the activity of Na(+)/K(+)-ATPase enzyme did not change, suggesting normal function. However, the damage to the liver was classified as moderate to severe. Cytoplasmic vacuolization, lipid accumulation, nuclear and cellular membrane alterations and glycogen depletion were found in the liver, suggesting a reduction in the liver function. The glyphosate in the RR formulation was classified as moderately toxic for P. mesopotamicus, and the severe damage in the liver may affect the detoxification and/or tissue repair process and contribute to fish death.     

The protective role of vitamin E on gill and liver tissue histopathology and micronucleus frequencies in peripheral erythrocytes of Oreochromis niloticus exposed to deltamethrin

Deltamethrin, is a commonly used pyrethroid pesticide. Vitamin E is a antioxidant that plays an important role in protecting cells against toxicity by inactivating free radicals generated following pesticides exposure. Therefore, it was evaluated whether deltamethrin induced histopathological changes and nuclear abnormalities using micronucleus test in Oreochromis niloticus, and the possible protective effect of vitamin E against deltamethrin inducing adverse effects in O. niloticus were investigated. Fish was fed with no pesticide+control diet, no pesticide+vitamin E-supplemented diet, 1.45μg/l deltamethrin+control diet, 1.45μg/l deltamethrin+vitamin E-supplemented diet for 30 days. Pesticide and diet quality made an impact on histopathological lesions. In treatments of deltamethrin, group fed with control diet showed much greater damage in comparison with group fed with vitamin E supplemented diet. Vitamin E decreased some histopathological changes induced by deltamethrin, but did not confer complete protection. Deltamethrin treatment has been shown to results in a significant increase in the frequency of micronucleus. However, coadministration of deltamethrin and vitamin E showed decrease in the frequency of micronucleus as compared to deltamethrin treated fish. Our results indicate that, the MN assay and histopathology can be used as bioassays for monitoring pollution in aquatic medium. On the other hand, it was observed that vitamin E decreased the genotoxicity and histopathological changes induced by deltamethrin.     

Toxic effects of the non-steroidal anti-inflammatory drug diclofenac. Part I: histopathological alterations and bioaccumulation in rainbow trout

Human and veterinary pharmaceuticals have been shown to occur in considerably high amounts in sewage treatment plant (STP) effluents and surface waters. The non-steroidal inflammatory drug diclofenac represents one of the most commonly detected compounds. Information concerning possible ecotoxicological risks of the substance are rather scarce. So far there are no data available on its possible effects in fish after prolonged exposure. In order to evaluate sublethal toxic effects of diclofenac in fish, rainbow trout (Oncorhynchus mykiss) exposed to diclofenac concentrations ranging from 1 microg/L to 500 microg/L over a 28 day period were investigated by histopathological methods. In addition, diclofenac residues in various organs were analyzed by means of gas chromatography/mass spectrometry (GC/MS). The histopathological examinations of diclofenac-exposed fish revealed alterations of the kidney such as an hyaline droplet degeneration of the tubular epithelial cells and the occurrence of an interstitial nephritis. In the gills, the predominant finding consisted in a necrosis of pillar cells leading to damage of the capillary wall within the secondary lamellae. The lowest observed effect concentration (LOEC) at which both renal lesions and alterations of the gills occurred was 5 microg/L. In contrast, the light microscopical examination of the liver, the gastro-intestinal tract, and the spleen did not reveal any histopathological alterations neither in diclofenac-exposed fish nor in solvent controls or control individuals. Chemical analysis showed a concentration-related accumulation of diclofenac in all organs examined. The highest amounts could be detected in the liver, followed by the kidney, the gills and the muscle tissue. Dependent on the diclofenac concentration used, the bioconcentration factors (BCF) were 12-2732 in the liver, 5-971 in the kidney, 3-763 in the gills, and 0.3-69 in the muscle respectively. From the present findings it can be assumed, that prolonged exposure in environmentally relevant concentrations of diclofenac leads to an impairment of the general health condition of fish.     

Acute toxicity and bioaccumulation of pesticide Diazinon in red tilapia (Oreochromis niloticus x Mossambicus albina)

Young red tilapias were exposed for 96 h to each one of 6 concentrations of the pesticide Diazinon in order to determine the pesticide's acute toxicity level. After the ascertaining the lethal concentration (LC50) at 96 h, a level 10 times lower was selected for the bioaccumulation study of the pesticide in male and female specimens exposed for 9 days. The elimination process was carried out for 10 days beginning right after the conclusion of the accumulation process. Analytical procedures were developed and used for the studies of acute toxicity and bioaccumulation of Diazinon in red tilapia. A lethal concentration [LC50 (96 h)] of 3.85 mg/L was found, and steady-state accumulation, at a concentration of 28.45 mg/kg, was reached at 7.72 days. In the elimination process a concentration of 0.29 mg/kg was found in tilapia tissue by the sixth day after the fish were moved to clean water, and it continued to decrease quickly toward nondetectable levels.     

Safety of emamectin benzoate administered in feed to Nile tilapia Oreochromis niloticus (L.)

Emamectin benzoate (EB) premix top-coated onto feed is extensively used to treat ectoparasitic crustacean infestations in aquaculture. This study evaluated the safety of EB-dosing in Nile tilapia Oreochromis niloticus at the recommended dose and dosage of 50 μg/kg biomass/day for 7 consecutive days (1X) and compared with control and 10 times the recommended dose (10X). Depletion of EB-residues in the edible muscle of 1X-dosed Nile tilapia was also studied. Mortality, behavioural changes, feed consumption, biomass, EB-residue depletion, and histopathological alterations in the kidney, liver and intestine were determined at slated intervals. Significant dose-dependent reduction in feed intake and biomass and insignificant mortalities were noted in 1X and 10X EB-dosed fish. In 1X EB-dosed fish muscle, the residues peaked on day 7 EB-dosing (9.72 ng/g) and decreased subsequently. Nevertheless, the residue levels were within the acceptable limit of the European Commission and the Canadian Food Inspection Agency even during the EB-dosing period. Histologically, tubule degeneration in the kidney, mild glycogen vacuolation in the liver, and loss of absorptive vacuoles, inflammation and disintegration of the epithelial layer in the intestine of Nile tilapia fed the 1X EB-diet were observed. The fish reverted back to their normal functions with time upon termination of oral-EB-dosing. This work contributed scientific data on the safety of EB particularly on the feed intake, growth reduction, mortality, histopathological alterations, and EB-residue levels in the edible tissues of Nile tilapia fed at the recommended dose and dosage, which suggested that EB-therapy might be reasonably risky in a tropical climate.     

Behavioral and morphological endpoints: as an early response to sublethal malathion intoxication in the freshwater fish,Labeo rohita

A short-term definitive test by the static renewal bioassay method was conducted to determine the acute toxicity (LC₅₀) of commercial-grade organophosphate insecticide, malathion (50% EC) on the freshwater fish, Labeo rohita. Carp fingerlings were exposed to different concentrations of malathion for 96 hours. The acute toxicity (LC₅₀) of malathion was found to be 4.5?µg/L. One tenth (1/10, 0.45?µg/L) of the acute toxicity value was selected as the sublethal concentration for subacute studies. The fish were exposed to sublethal concentration for 1, 5, 10, and 15 days and allowed to recover in toxicant-free medium for 15 days. Behavioral responses and morphological deformities were studied in the experimental tenures. Fish in toxic media exhibited irregular, random, circular swimming movements, hyperexcitability, loss of equilibrium, and sinking to the bottom. Caudal bending was the prime morphological malformation. The behavioral and morphological deformities were due to inhibition of acetylcholinesterase (AChE) activity. Inhibition of AChE activity results in excess accumulation of acetylcholine in cholinergic synapses, leading to hyperstimulation and cessation of neuronal transmission (i.e., paralysis). The carp were found under stress, but mortality was insignificant at the sublethal concentration tested. Impaired behavioral responses and morphological deformities were observed during recovery. This may be a consequence due to inhibition of brain and muscular AChE by malaoxon, via the biotransformation of sequestered malathion.