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Effect of Exposure to Potassium Permanganate on Stress Indicators in Channel Catfish Ictalurus punctatus
Journal of the World Aquaculture Society
Abstract
Juvenile channel catfish Ictulurus punctatus were exposed to 1× (0.44 mg/L), 3× (1.32 mg/L), or 5× (2.19 mg/L) the recommended therapeutic concentrations of waterborne potassium permanganate (KMnO4) for 36 h to determine the toxicity of the chemical. The fish were observed for 14 d after exposure. Gill, liver, and blood samples were collected before exposure, at 12, 24, and 36 h of exposure, and at 48-h intervals for 14 d thereafter. Analysis of homogenized gill tissue showed a transient increase in manganese content that quickly disappeared once exposure was discontinued. Fish exposed to the 3× and 5× concentrations of KMnO4 experienced 9 and 50.6% mortality, respectively. Plasma cortisol was elevated more than ten-fold at the 5× concentration. Both plasma chloride and osmolality were significantly reduced at the 3× and 5× concentrations but were unchanged at the 1×. Packed cell volumes (PCV) of whole blood rose significantly in response to 3× and 5× concentrations of KMnO4 Mortality may have been the result of blood electrolyte depletion as indicated by increased PCVs, loss of chloride, and reduced osmolality. All stress indicators measured, except PCV at the 5× concentration, were indistinguishable from unexposed controls within 48 h after exposure was discontinued. At the l× concentration (the concentration most like that employed in a disease treatment) no changes were observed in any stress indicators measured suggesting that KMnO4 may be safely used as a disease therapeutant for channel catfish.
... Potassium permanganate, a strong oxidizing agent, exhibits potent antimicrobial activity against bacteria, fungi, viruses, and protozoans by altering their cell walls and interfering with DNa structures (Duncan, 1974;lay, 1971;Mahgoub et al., 2020;straus & Griffin, 2002). it has been used for centuries in the treatment and prevention of fish diseases. ...
... the elevation in glucose levels can be attributed to the chemical stress induced by KMnO 4 , which leads to the secretion of catecholamines and subsequent enhancement of glycogen breakdown in the liver, thereby raising blood glucose levels in the affected fish. Griffin et al. (2002) also reported an increase in blood glucose levels in channel catfish following exposure to KMnO 4 . in our study, rohu exposed to different concentrations of formalin exhibited a noteworthy reduction in serum protein levels. ...
The present study aimed to elucidate the suitability of formalin and KMnO4 as therapeutics for fish diseases in Indian major carp, Labeo rohita, while considering their impact on fish stress levels. Acute toxicity tests revealed that the 96-hour LC50 values for formalin and KMnO4 were 66.58 ppm and 2.89 ppm, respectively. Sub-lethal concentrations of formalin (6.65 ppm, 3.32 ppm, and 2.21 ppm) and KMnO4 (0.289 ppm, 0.145 ppm, and 0.096 ppm), along with control groups, were administered to the fish for different exposure periods (24, 48, 72, and 96 hours) and different hematological, biochemical, and immunological parameters were analyzed. The findings demonstrated that formalin exposure resulted in a significant decrease (p < 0.05) in hematological parameters, immunological parameters, and serum protein levels. Conversely, formalin exposure led to significant increases (p < 0.05) in serum glucose, SGOT, SGPT, and ALP levels. In contrast, KMnO4 exposure significantly decreased (p < 0.05) hematological parameters and serum protein levels, while significantly increasing (p < 0.05) immunological parameters. To evaluate curative efficacy, challenge studies were conducted using three sub-lethal concentrations of formalin and KMnO4 against Aeromonas hydrophila (ATCC 7966) infection. Based on the aforementioned results, the recommended doses of formalin and KMnO4 were found to be 6.65 ppm and 0.289 ppm, respectively.
... Both plasma glucose and lactate were within reference ranges reported by Tavares-Dias and Moraes (2007), indicating fish did not deviate greatly from normal levels, regardless of trematode exposure. Trematode infection did result in an overall decrease in osmolality (245 ± 4.8 mmol/kg) compared to non-infected fish (275 ± 1.8 mmol/kg), with levels in exposed fish (245 ± 4.8 mmol/kg) decreased compared to previous studies of healthy fish (Eckert et al., 2001;Griffin, Davis, Darwish, and Straus, 2002). Decreased osmolality could be due to blood dilution, as there was a significant drop in RBC concentration during the encapsulation period and parasite-associated hemorrhage. ...
... Decreased osmolality could be due to blood dilution, as there was a significant drop in RBC concentration during the encapsulation period and parasite-associated hemorrhage. Decreased osmolality is a typical response resulting from a loss of electrolytes in channel catfish exposed to chemical and bacterial stressors, although this has not been studied as a response to parasitic infection (Griffin, Davis, Darwish, and Straus, 2002;Welker, Lim, Yildirim-Askoy, and Klesius, 2007). Decreased osmolality could indicate a long-term lowlevel response to parasite infection in both channel and hybrid catfish, even after the encapsulation process is complete. ...
The trematode Bolbophorus damnificus is associated with reduced production in farm-raised catfish in the southeastern United States. Previous research demonstrated that even mild outbreaks, which may go unnoticed by producers, can result in >60% reduction in net return due to decreased feeding and trematode-induced mortality. While infectivity rates in channel (Ictalurus punctatus) and hybrid catfish (I. punctatus x I. furcatus) are similar, hybrid catfish experience lower mortality when exposed to comparable numbers of Bolbophorus cercariae than channel catfish cohorts. This study compared physiological responses in channel (21.4 ± 0.93 g) and hybrid (27.5 ± 2.63 g) catfish fingerlings exposed to 450 cercariae/L. Fish were sampled over the next 49 days for hematocrit, hemoglobin, red blood cell (RBC) concentration, plasma glucose, plasma lactate, and plasma osmolality. Exposed channel and hybrid catfish experienced a dramatic drop in hematocrit, hemoglobin, and RBC concentration during the peak mortality window associated with metacercarial development, but recovered afterwards, suggesting an anemic response to the development of the parasite and subsequent recovery once metacercarial encapsulation is complete (~15 days post-exposure). There were no differences over time in any of the plasma parameters measured, but there was an overall decreased osmolality in both exposed groups, suggesting a prolonged low-level stress response to infection. There was high mortality in the exposed channel catfish groups from days 9 to 15 post-infection, consistent with previous studies. Comparably, hybrids appeared healthy and active throughout the trial with only negligible mortality. In all trials, infected fish presented clinical signs consistent with B. damnificus infection and all exposed fish had visible metacercariae below the skin. There was a substantial anemic response in both catfish types, suggesting the physiological response to B. damnificus infection may not differ between channel and hybrid catfish and the significant differences in mortality may be attributed to survivor bias, hybrids greater tolerance of the anemic state or other unidentified factors. The biological and economic implications of these findings are unclear, but the behavioral differences observed between the two fish groups in reponse to B. damnificus, coupled with reduced mortality in hybrids, supports previous work indicating hybrids are more tolerant of B. damnificus infection and outbreaks in hybrid catfish may not yield the same deleterious effects as channel catfish.
... 20,26,[28][29][30][31]37,50 Examples of other compounds investigated for toxicity under natural or experimental conditions in channel catfish include copper sulfate, cyclopiazonic acid, potassium permanganate, and methyl mercury. 17,19,22,39 This report details the clinical findings, pathology, and diagnostic investigation into a prolonged mortality event involving channel and blue catfish exposed to pyrethroid insecticides in an outdoor, recirculating display system at a public aquarium. ...
Over the course of an approximately 11-month period, an outdoor, freshwater, mixed species, recirculating, display system at a public aquarium experienced intermittent mortalities of channel catfish ( Ictalurus punctatus) and blue catfish ( I. furcatus). Catfish acutely presented for abnormal buoyancy, coelomic distention, and protein-rich coelomic effusion. Gross lesions typically involved massive coelomic distension with protein-rich effusion, generalized edema, and gastric hemorrhage and edema. Microscopically, primary lesions included renal tubular necrosis, gastric edema with mucosal hemorrhages, and generalized edema. Aerobic culture and virus isolation could not recover a consistent infectious agent. Intracoelomic injection of coelomic effusion and aspirated retrobulbar fluid from a catfish into naïve zebrafish (bioassay) produced peracute mortality in 3 of 4 fish and nervous signs in the fourth compared with 2 saline-injected control zebrafish that had - no mortality or clinical signs. Kidney tissue and coelomic effusion were submitted for gas chromatography tandem mass spectrometry by multiple reaction monitoring against laboratory standards, which detected the presence of multiple pyrethroid toxins, including bioallethrin, bifenthrin, trans-permethrin, phenothrin, and deltamethrin. Detection of multiple pyrethroids presumably reflects multiple exposures with several products. As such, the contributions of each pyrethroid toward clinical presentation, lesion development, and disease pathogenesis cannot be determined, but they are suspected to have collectively resulted in disrupted osmoregulation and fluid overload due to renal injury. Pesticide-induced toxicoses involving aquarium fish are rarely reported with this being the first description of pyrethroid-induced lesions and mortality in public aquarium-held fish.
... The definitive tests (1, 2 and 3) were performed in accordance with the protocols published by the American Society for Testing and Materials (Griffin et al., 2002). ...
The objective of this study was to evaluate the acute toxicity of formalin and its level of therapeutic safety in early stages of Lophiosilurus alexandri. Experiment 1, larvae 7 days after hatching (DAH) were exposed to 43.2, 86.4, 172.8, 345.6, 691.2, 1404.0 mg/L of formalin. Experiment 2, juveniles with 22 DAH exposed to 54, 108, 216, 432, 648 mg/L. Experiment 3, 45 DAH exposed to 86.4, 172.8, 345.6, 691.2, 1036.8 mg/L. The experiments had a control without addition of formalin and all were carried out in duplicate. The LC50-12 h were: Experiment 1 = 108.86 mg/L; 2: 152.74 mg/L; 3: 244.38 mg/L of formalin. The respective safety levels were: Experiment 1 = 66.22 mg/L (1 h), 10.89 mg/L (12 h); 2 = 49.17 mg/L (2 h), 15.27 mg/L (12 h); 3 = 68.89 mg/L (2 h), 24.44 mg/L (12 h). The results showed that the developmental stage influenced the sensitivity of animals to formalin.
... Mn via potassium permanganate (KMnO 4 ) has been in use for removing parasites from fish, reducing fish diseases during fish culture and as disinfectant in fish hatcheries since 1893 [76]. Unfortunately, at higher concentration, it ceases to perform physiological functions but rather inflict deleterious lesions that may lead to mortality or morbidity in aquatic species [36]. The trio of Cd, Pb and Mn exists at Fig. 1 Frequency of micronucleated erythrocytes in peripheral blood of C. gariepinus exposed to Cd, Pb, Mn and CPM. ...
Heavy metals are ubiquitous environmental and occupational genotoxicants with different absorbability and toxicokinetics towards increasing genetic damage, neoplasm and cell death. Aquatic organisms are exposed to individuals and/or mixtures of these metals. This study investigated the potentials for cadmium(II) (Cd), lead(II) (Pb), manganese(II) (Mn), and their mixture (CPM) to induce cytogenotoxicity in Clarias gariepinus (Family: Clariidae). Clarias gariepinus was exposed to six concentrations ranging from 0 to 1600 mg/L, selected from range finding tests, to evaluate the 96 h acute toxicity for the individual metals and CPM. Fish were exposed to sub-lethal concentrations (6.25, 12.5 25, 50, and 100% of the 96 h LC50) of each metal and their mixture for 7 days to investigate micronucleus (MN) and abnormal nuclei (NAs) in the peripheral blood erythrocytes. Fish were exposed to borehole tap water and 0.01 mL/L of Benzene as negative and positive controls respectively. The tested metals induced toxicity in the order CMP > Cd > Pb > Mn, with CPM (LC50 = 40.6 mg/L) being 11.5 times more toxic than Mn (LC50 = 478.2 mg/L), the least toxic metal, to juvenile catfish. All the tested metals induced significant increase in frequencies of MN and NAs. The induced MN and NAs were in the order CMP > Cd > Mn > Pb. Fragmented and necrotic cells were common NAs in fish treated with 50 and 100% of Cd and CPM, suggesting that severely damaged cells were eliminated by programmed cell death (apoptosis) and/or accidental cell death (necrosis). Antagonistic interaction among the composite mixture of CPM provoked greater genomic instability and cytotoxicity in fish. Significant increase in MN and NAs in exposed fish suggest increased genomic instability which may lead to increase health defects including neoplasms and genetic related disorders, cell dysfunction and/or cell death.
... cod Gadus morhua L.: Puvanendran & Brown, 2002). Griffin et al., 1999Griffin et al., , 2002Yildiz & Pulatsu, 1999;Sorum & Damsgard, 2004)). ...
Choosing fish as subject matter, this chapter attempts to challenge the ‘thoroughgoing speciesism’ (Beirne 1999) inherent in the mammalian-centric animal abuse literature. To do this, it draws on research in marine biology and animal cognition to philosophically establish that fish are moral agents, and ‘subjects-of-a-life’ (Regan 1983), on par with mammals, and thus, worthy of more in-depth consideration. Then, using the Marine Aquarium Fish Trade as a case study, this chapter proposes an integrated theoretical framework within green criminology that strengthens the political economic ‘treadmill of production’ theory (see Lynch et al. 2013) by incorporating a an analysis of the ‘cultural grease’ that ensures the treadmill’s smooth operation. It outlines the ideological work of the Association of Zoos and Aquariums (AZA) and specifically considers how, through its public aquariums and organizational behavior, the AZA and its member aquariums facilitate cultural narratives and silences conducive to ecologically destructive anthropocentric capitalism and the trade in marine fish. Finally, the chapter outlines the specific instances and macro-patterns of environmental degradation these narratives facilitate through the treadmill of production itself: from the widespread destruction of coral reef habitats in Southeast Asia, to harm induced by transportation, to global warming, resulting, ultimately, in mass marine-theriocide.
Concerns for the welfare of fish during the farming/production process is in its infancy when compared to other species. This is due to disputes in the interpretation of characteristics that suggest awareness in fish, a concern that is somewhat widespread among consumers and producers. Through questionnaires, this study aimed to highlight what the members of a fishermen's association (that farm Tilapia and Robalo Peva) understand about the welfare of fish, and whether it is considered during the production process. In addition, although there are still many controversies, this perception has been changing in recent years, in part due to anatomical, physiological and behavioral evidence that suggest fish are sentient (are aware of sensations, have subjective feelings). Moreover, as the consumer has become aware of the issues, concern for animal welfare has increased, leading to a need for the market to adapt to these requirements.
Static 96 h bioassays were conducted on milkfish fingerlings at concentrations ranging from 1.00 to 1.80mg/l KMnO4. Histopathological analyses of gills, liver, and kidney tissues revealed significant changes even in non-lethal concentrations tested. Damage became severe with in-creasing concentration and longer exposure to the chemical. Partial to complete recovery was observed in gills, liver, and kidney cells of fish exposed to KMnO4 for 96h and then maintained in KMnO4-free seawater for 240h.
This volume aims to review and present research on acid waters and their effects on aquatic animals. Starting initially with the environment in order to assess why the problems have arisen in particular areas, the volume then deals with field and survival studies on invertebrates and vertebrates and examines the extent of the biological problem and the attempts which have been made to relate water quality and the susceptibility of animals. Major advances in this area have included the realization that declining populations are often the result of acid waters and their interactions with traces of other ions and that these situations produce the most severe physiological problems. The natural progression of environmental and field studies, toxicity and survival tests provide the background information for the physiological studies which follow. These form the major component of the book and they seek to analyse the toxic effects of acid waters and trace metals on acid-base balance, respiration, ionic balance together with cardiovascular and endocrinological effects.
Potassium permanganate is an oxidant heavily used in fish culture. The effects of this compound were examined utilizing molecular (Metallothionein) and whole animal endpoints following an 8-week exposure to nominal concentrations of 0.5 (daily) and 1.0 and 2.0 mg/L (on alternate days) of potassium permanganate (PM). In order to measure MT, a complementary DNA clone of metallothionein (MT) was cloned and sequenced from the liver of channel catfish treated with a single injection of cadmium chloride (10 mg/kg). The cDNA was obtained by reverse transcriptase polymerase chain reaction (RT-PCR), using 3* rapid amplification of cDNA ends (RACE) technique. No significant correlation was observed with gill MT expression or sublethal endpoints indicative of toxicity (weight, length, condition index [CI], or liver somatic index [LSI). MT mRNA expression in gill was significantly reduced only after 8 weeks in the 2.0 mg/L treatment. Decreases in CI were observed in males at all time points after 4 weeks, at the 2.0 mg/L treatment concentration, with a NOEC of 1 mg/L. Reductions in LSI that were not dose dependent were also observed in both males and females throughout the 8-week study and no consistent reduction in weight gain or length was observed. These data demonstrate that minimal changes in sublethal effects occur in fish following 0.5‐2.0 mg/L PM treatment after 4 weeks, but recovery from adverse effects is observed by 8 weeks, suggesting that acute (typically less than 1 week) treatment of channel
Carbohydrate metabolism variables of Oreochromis mossambicus were investigated after acute and chronic sublethal manganese exposure. The sublethal concentrations were determined from the LC50 value of manganese. After the exposures, the fish were carefully netted and blood was drawn from the caudal aorta. The differences in the values of carbohydrate metabolism variables of exposed fish were measured against control values and statistically analysed to prove statistically significant differences in variable values, caused by the metal pollutant (P < 0.05). The results obtained showed changes in the carbohydrate metabolism variables (glucose, lactate, glucose-6-phosphate dehydrogenase and pyruvate kinase concentrations). These alterations are produced as a result of increased levels of cortisol and catecholamines, as well as hypoxic conditions. The latter induce hyperglycemia and increased lactate levels. Hypoxia may be a result of the damaging effect of manganese on the gills after exposure. The enzymes involved in the carbohydrate metabolism are sensitive to metal exposure and therefore enzyme concentrations fluctuated after the exposure to manganese. Enzyme function plays an important role in the catalysing of chemical reactions in an organism and the disturbance thereof could lead to death. Fish enzyme levels are therefore important biomarkers in the event of metal pollution in a water source.
Plasma-corticosteroid concentrations in resting channel catfish Ictalurus punctatus held at 21 C varied only slightly during a 24-hour period; further, increases in hormone concentrations induced by confinement stress were independent of time of day and photoperiod. Temperature strongly affected both resting corticosteroid concentrations and the dynamics of hormone secretion when fish were stressed. Resting concentrations were greatest in fish acclimated to 5 and 10 C (25–29 ng/ml), sharply lower in fish held at 15, 20, or 21 C (5–9 ng/ml), and intermediate in fish maintained at 25, 30, or 35 C (12–13 ng/ml). Hormone concentrations increased when fish were stressed by confinement. Corticosteroid concentrations hardly changed in fish held at 5 or 10 C, but increased markedly in fish at higher temperatures; in addition the response was more delayed at the lower temperatures.
The 96-h LC50's for potassium permanganate (KMnO4) ranged from 0.750 mg/liter with channel catfish, Ictalurus punctatus, to 3.60 mg/liter with goldfish, Carassius auratus, in laboratory tests. The toxicity of KMnO4 to fish is greatest in water of lower temperatures, in harder water, or in higher pH water. KMnO4 is effective for detoxifying the fish toxicant antimycin in laboratory waters of pH 6.5 to 9.5. The half-life for antimycin exposed to 1.0 mg/liter of KMnO4 ranges from 7 to 11 minutes in the different pH waters at 12 C.
Adult channel catfish Ictalurus punctatus were exposed to waterborne potassium permanganate for 12 weeks to determine if such exposure would alter the manganese content of axial muscle or liver tissue. Continuous exposure to 0.5 mg KMnO4/L or exposure to 1 or 2 mg KMnO4/L on alternate days did not cause a significant increase in manganese in axial muscle or liver tissue. The mean (±SE) concentration of manganese in axial muscle of unexposed controls was 0.262 ± 0.018 mg/kg (wet weight). Means of manganese concentrations in axial muscle of the three exposure groups during the 12 weeks of exposure were 0.289 ± 0.021 mg/kg, 0.269 ± 0.018 mg/kg, and 0.239 ± 0.013 mg/kg for 0.5 (continuous), 1, or 2 mg/L (alternate days), respectively. At specific sampling times there were differences between controls and exposure groups; however, no trend toward higher or lower manganese concentrations in muscle could be detected within groups. The mean (±SE) concentration of manganese in liver tissue of controls was 1.67 ± 0.09 mg/kg (wet weight). Manganese concentrations in liver tissue of the three exposure groups were 1.57 ± 0.07 mg/kg, 1.68 ± 0.08 mg/kg, and 1.58 ± 0.10 mg/kg, for 0.5 (continuous), 1, or 2 mg/L (alternate days), respectively. Manganese was thought to accumulate in liver tissue, however, there were no statistically significant differences between those groups and the controls. Results suggest that potassium permanganate used as a waterborne disease therapeutant for channel catfish does not alter manganese content of edible muscle of channel catfish and should not present any hazard to human consumers.
A rapid, precise, and accurate method for the determination of aluminum in part-per-billion concentrations in biological materials using graphite-furnace atomic absorption spectroscopy has been developed. In order that the necessary accuracy and precision for the analysis of aluminum in bone and brain tissue could be obtained, reduction of laboratory environmental contributions to the aluminum blank was required. Use of a closed-vessel microwave digestion system and a clean room for sample preparation accomplished this goal by reducing Al concentrations in the digestion blanks from 10 ppb to 1 ppb. Digestion time was decreased from many hours to several minutes, and the amount of acid required for digestion was reduced by 70%. Using less nitric acid improved precision in the analyzed solutions by significantly extending the lifetime and consistency in performance of the graphite tube atomizer.
Adult channel catfish Ictalurus punctatus were continuously exposed to waterborne copper sulfate added at concentrations of 1.7, 2.7, or 3.6 mg/L for 10 weeks. Overall, there were no significant differences in the copper content of channel catfish axial muscle during the exposure period, and no significant copper accumulation resulted from exposure. Significantly higher concentrations of copper were present in liver tissue of catfish in all exposed groups 2 weeks after exposure to waterborne copper sulfate began. Extent of copper accumulation in the liver was gender and dose related, with higher concentrations in males at the highest dosage level. Exposures to waterborne copper sulfate were discontinued after 10 weeks, and copper concentrations in liver tissue subsequently returned to levels indistinguishable from controls in 4-8 more weeks. Results indicate that copper sulfate used as a waterborne disease therapeutant for channel catfish does not alter copper content of edible muscle of channel catfish and should not present any hazard to human consumers.