Effect of Heavy Metals On Fishes: Toxicity and Bioaccumulation
Effect of Heavy Metals On Fishes: Toxicity and Bioaccumulation
Effect of Heavy Metals On Fishes: Toxicity and Bioaccumulation
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ABSTRACT
Heavy metal pollution is a serious problem for the environment due to their toxicity, persistency, bioaccumulation,
and bio magnifications property. Heavy metal contamination in the environment can occur from different natural
and anthropogenic sources. The natural sources of heavy metals are mainly volcanic eruption and weathering of
metal-bearing rocks, while the anthropogenic sources of heavy metals include agricultural and industrial activities,
combustion of fossil fuel and gasoline, waste incinerators, mining, etc. The mobilization of these heavy metals to
the aquatic ecosystem alters the physicochemical property of water which is hazardous for aquatic organisms. Heavy
metals mainly enter the fish body through gills, body surface and digestive tract during ingestion of metal accumulated
food materials. Cadmium, chromium, nickel, arsenic, copper, mercury, lead and zinc are the most common heavy
metal pollutants that cause severe toxicity in fishes. Development of oxidative stress is the fundamental molecular
mechanism of metal toxicity. The stress weakens the immune system, causes tissue and organ damage, growth defect
and reduces reproductive ability. The rich source of high-quality protein filled with vitamins and omega-3 fatty acids
encourage the human being to uptake fish as a major food source. So, accumulated heavy metals in the fish tissues
directly transfer to the human body and cause toxic effects to expedite various diseases. Therefore, it is necessary to
discuss the sources of heavy metals and their toxic effect on fish health to enforce the law and legislations regarding
their protection in the aquatic environment and also to save human life.
Keywords: Heavy metal; Aquatic ecosystem; Bioaccumulation; Toxicity; Oxidative stress
INTRODUCTION the microbiological balance and reduced soil fertility [6]. The
heavy metals can easily dissolved in the aquatic environment and
Environmental pollution is one of the major challenges for human subsequently enter into the body of aquatic organisms [7]. In the
society nowadays [1]. Due to the fast-growing industries, increased course of the food chain, those metals then enter into the body
energy demand and careless destruction of natural resources of higher animals. Bioaccumulation of toxic heavy metals in the
from the last few decades environmental pollution is increasing different tissues may harm animal health and causes damage to
day by day [2]. Different organic and inorganic toxic materials their normal physiological processes [8]. Heavy metal toxicity
are constantly releasing from various natural and anthropogenic drastically affects the rate of survivability and reproductive capacity
sources in the soil and aquatic ecosystem. Among them, heavy of the organisms. Some of these have been reported to be highly
metals are playing a major role in environmental pollution, not carcinogenic, mutagenic and teratogenic depending on the species,
only for their toxic nature but also possessing the potentiality of dose and exposure time [9].
bioaccumulation in the food chain [3]. Heavy metals are mostly
releasing from domestic and agricultural waste products, industrial Aquatic biota directly exposed to the heavy metals that dissolved
waste materials, combustion of fossil fuels, mining, waste water in water or present as sediment in the water body [10]. Being the
treatment plants to the natural ecosystem [4]. top consumers of the aquatic ecosystem fishes are affected most
[11]. Heavy metal toxicity sometimes damages the nervous system
Since heavy metals are persistent in the natural ecosystem, once of fish that affects the interaction of fish with its environment [12].
enter into the living organism, it can accumulate inside. The heavy Humans are omnivorous and exposed to toxic heavy metals by
metals that contaminate the soil are easily taken up by the plants different food items such as fish, vegetables and cereals. Therefore,
and lead to different adversity e.g. chlorosis, growth inhibition, the heavy metal contamination in the body of aquatic organisms
defect in water balance and photosynthesis, senescence, and finally or plants can biomagnified and persist in the food chain, results in
death [5]. The soil contamination of heavy metals also affects
Correspondence to: Nimai Chandra Saha, Department of Zoology, Fisheries and Ecotoxicology Research Laboratory, University of Burdwan, Burdwan,
West Bengal, India, Tel: +91 8617482954; E-mail: [email protected]
Received: May 12, 2021; Accepted: May 28, 2021; Published: June 05, 2021
Citation: Garai P, Banerjee P, Mondal P, Saha NC (2021) Effect of Heavy Metals on Fishes: Toxicity and Bioaccumulation. J Clin Toxicol. S18:001.
Copyright: © 2021 Garai P, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which
permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
transfer to the human body [13]. Heavy metal toxicity has become carbonate, cadmium nitrate and cadmium cyanide are commonly
an important global threat for fish consumers [14]. found [31]. Cadmium is released in the aquatic ecosystem from
different natural and anthropogenic sources. Natural sources of
cadmium are from the earth's crust and mantle by the volcanic
The present review aims to discuss the bioaccumulation and eruption and weathering of rocks. Whereas anthropogenic sources
toxic effect of different heavy metals like Chromium, Cadmium, include combustion of fossil fuels, fertilizers, agricultural waste and
Copper, Lead, Nickel, Arsenic, Mercury and Zinc on fish health, so industrial use (plastic stabilizers, pigment, batteries, electroporating
that necessary steps can be taken to minimize the impact of these industries) which contaminate the water body [32,33]. The flora
metal elements in our ecosystem. and fauna of water body uptake water soluble or sediment form of
cadmium compounds, which indirectly enter into the fish body in
Chromium (Cr) course of the food chain [34]. Whereas fishes uptake water dissolved
Chromium is one of the most common trace elements found in the free ionic form of cadmium directly through gill, gastrointestinal
earth's crust and seawater [15]. This element is not present in the tract and skin [35].
environment as pure metal form, but present in divalent (Cr2+), Cadmium is considered as a nonessential element and causes
trivalent (Cr3+) or hexavalent (Cr6+) oxidation states. Among severe toxicity to fishes. It inhibits the electron transfer chain in
these different forms, Cr3+ and Cr6+ are the most stable forms mitochondria and stimulates Reactive Oxygen Species (ROS)
[16,17]. Cr3+ oxidation state is less toxic due to low membrane production [36]. A low level of cadmium exposure induced DNA
permeability, non-corrosiveness nature and minimum power of bio damage in Cyprinus carpio [37]. Trans-epithelial calcium influx in
magnifications in the food chain. Cr6+ state is more toxic because rainbow trout gill was found to be inhibited by Cd+2 [38]. Micro-
of its strong oxidative potentiality and ability to cross the cell nucleated and bi-nucleated cells formation in blood, gills and liver
membrane [18]. In an aquatic ecosystem, chromium toxicity occurs were observed in subchronic cadmium chloride exposure in fish
from different anthropogenic sources such as leather tanneries, [39,40]. Reported histopathological alteration like fatty vacuolation
metal processing, petroleum refining, textile manufacturing, alloy in the liver; necrosis in hepatocytes; congestion of sub mucosal
preparation, wood preserving etc. [19,20]. blood vessels in the intestine and glomerular shrinkage and necrosis
The toxicity of chromium to aquatic organisms is dependent upon in kidney tissue of Tilapia (Oreochromis niloticus). Fish exposed to
various biotic factors like age, developmental phase and type of cadmium showed a differential haematological response. After 8
species; and abiotic factors like pH, temperature and alkalinity weeks of exposure to 150 µg/L of cadmium in American eel fish
of water. Initial exposure of fish to chromium showed different (Anguilla rostrata), lead to anaemia due to reduction in haemoglobin
behavioural changes i.e. uneven swimming, mucous discharge, and erythrocyte counts. Significant increase in leukocyte and large
change in body colour, loss of appetite etc., [21]. Chronic exposure lymphocytes count was also observed after cadmium exposure [41].
of chromium at a concentration of 2-200 µmol/L on Cyprinus The level of glycogen reserve in muscle and liver was decreased
carpio showed cytotoxicity, decreased mitogen-induced lymphocyte significantly and blood glucose level increased in Cyprinus carpio,
activation and phagocyte functions [22]. Blood coagulation time exposed to sublethal concentration of cadmium [42]. Cadmium
was decreased in the Tilapia sparrmanii exposed to chromium, is an endocrine disrupter and an inhibitor of vitellogenesis,
which reflects by internal bleeding with an increase of pH value observed in rainbow trout Oncorhynchus mykiss [43]. Exposure to
[23]. Accumulation of chromium in the tissue of Indian major cadmium chloride affected the gonad function and sexual maturity
carp Labeo rohita decrease total protein and lipid content in in common carp Cyprinus carpio [44]. Cadmium exposure to
the muscle, liver and gill [24]. The depletion of liver glycogen the larvae of ide Leuciscus idus showed body malformations and
content was observed in a freshwater teleost Colisa fasciatus, on reduced embryonic survival rate due to death in newly hatched
chromium exposure [25]. In rainbow trout, Salmo gairdneri, Cr6+ larvae [45].
toxicity showed osmoregulatory and respiratory dysfunction at Cadmium accumulation is a serious environmental concern
pH 7.8 and 6.5 [26]. Chronic exposure of chromium to Chinook because of its slow rate of excretion. The highest level of cadmium
salmon caused DNA damage, microscopic lesions, physiological bioaccumulation is found in the liver, kidney and gill and lowest
abnormalities, and reduction in growth and survival rate [27]. In level in the skin. Gill is the most efficient organ for cadmium
rainbow trout Salmo gairdneri, embryo hatching and the growth detoxification [46]. Cadmium is considered is one of the most
of fish were affected after chromium exposure at a concentration toxic heavy metals for aquatic organisms because of its high rate of
of 2 mg/L [28]. bioaccumulation.
Bioaccumulation of chromium varies differentially in various Copper (Cu)
tissues of fish (Table 1). The highest accumulation of chromium is
found in gills, liver and kidney and very low concentration is found Copper pollution in the freshwater ecosystem occurs due to
in the muscle tissue [29]. extensive use of fungicides, algaecides and insecticides in the
agricultural field and then discharge of the waste materials to the
Cadmium (Cd) water body. Other than that, copper toxicity also occurs from the
Cadmium is a trace element present in the earth's crust on an electroplating industry, metal refining industry, plastic industry,
average concentration is about 0.1-0.5 ppm and is commonly found mining, sewage sludge, atmospheric deposition etc. [47,48].
in association with zinc, copper and lead ores. In ocean water, Copper is an essential trace element and micronutrient, important
the average concentration is between 5-110 mg/L and in surface for the growth and metabolism of living organisms. In fish and
water and ground water is usually <1 µg/L [30]. Element form of other vertebrates, copper is the key constituent of many metabolic
cadmium is not available in nature. Instead, compound forms e.g. enzymes and glycoprotein. It is also essential for haemoglobin
cadmium chloride, cadmium oxide, cadmium sulphide, cadmium synthesis and nervous system function [49,50]. But, at higher
Table 1: Heavy metal bioaccumulation in different tissues or organ of fish-ranked in decreasing order.
Liver>gills>blood>muscle>skin>br
Clariasbatrachus Kumar et al., 2012
Arsenic ain
concentration, copper causes toxic effect on living organisms [51]. immunological parameters was observed in Tench (Tinca tinca)
Copper causes toxicity to freshwater fish at a concentration ranging lethal and sublethal exposure to lead [74].
from 10-20 ppb [52]. Toxicity of copper to aquatic life is dependent
on several factors, i.e. water hardness, pH, anions and Dissolved Lead bioaccumulation in fish mainly occurs in the liver, spleen,
Organic Carbon (DOC). Fish uptake copper mainly through the kidney and gills [75]. Lead bioaccumulation also affected free
dietary route or ambient exposure [53]. Exposure to waterborne locomotion and induced morphological deformities in Chinese
copper on freshwater fish induced oxidative stress response [54]. sturgeon, Acipenser sinensis [76].
Chronic toxicity of copper in fish causes poor growth, shortening Nickel (Ni)
of life span, decreased immune response, and fertility problems
[55]. Copper toxicity in the gill of teleost fish (Oreochromis Nickel is a very abundant trace element found in the environment,
niloticus), showed induction in apoptosis [56]. In Cyprinus carpio, present in combination with oxygen or sulphur. Nickel is released
copper sulfate exposure showed biochemical and morphological into the environment from both natural and anthropogenic sources.
changes in the liver tissue [57]. Micronuclei and binuclei formation The element is discharged from industries during nickel mining
was induced in blood erythrocytes, gill epithelial cells and liver and transformation of new nickel into alloys or nickel compounds.
cells of fish, after subchronic exposure to copper sulphate. Copper Nickel is also released from coal-burning power plants, oil-burning
impaired complex fish behaviours such as, social interaction, power plants and trash incinerators [77].
avoidance of predators and reproductive behaviour that are Nickel is an essential element for many organisms at low
important for survival. Copper toxicity to Mytilus edulis lead to a concentration, but at high concentration, it causes toxicity [78].
decrease in heart rate and cardiac function [58]. Copper exposed Nickel toxicity in fishes is dependent upon different physiochemical
Oreochromis mossambicus showed an increase in RBC count, properties of water like pH, ionic strength, temperature, hardness,
haemoglobin content and hematocrit value [59]. This element is Dissolved Organic Carbon (DOC) etc. [79]. Exposure to nickel
neurotoxic to fish and interferes with the function of olfactory chloride in Nile tilapia showed abnormal swimming behaviour,
neurons [60]. Copper exposed zebrafish larva became greater rapid opercular movement, respiratory disorder and lesions in
sensitive than embryonic and adult stage and showed lateral line the skin. Nile tilapia exposed to nickel also showed a change in
dysfunction [61]. The larvae of goldfish Carassius auratus showed blood parameters like, increase of RBC count and a decrease of
a high rate of body deformities and mortality on copper exposure haemoglobin and WBC counts [80]. Histopathological changes in
[62]. Copper accumulates at the highest concentration in the different tissues like gill, kidney, liver and intestine were observed
liver and less concentration in the gill and body flesh of fish [63]. in nickel exposed freshwater fish Hypophthalmichthys molitrix.
Bioaccumulation of this trace element influenced the oxidative The fusion of gill lamellae, necrosis of hepatocytes, blood vessels
metabolism, lipid peroxidation and protein content in carp tissue degeneration, hypertrophy, vacuolation, pyknotic nuclei and lesion
[64]. were observed in the liver tissue. Hyperplasia and degeneration of
Lead (Pb) tubular cells in kidney tissue were also observed on nickel exposure
[81]. In chronic and acute exposure of nickel to freshwater fish
Lead is considered as one of the most hazardous heavy metals, Oreochromic niloticus, reduced ATPase activity in the brain [82].
which is naturally present in the environment, in combination with Nickel exposure in freshwater fish Prochilodus lineatus, affected
other elements i.e. PbS, PbSO4 and PbCO3.The concentration the antioxidant defence system in the liver and induced DNA
of lead in the environment is very much increased by different damage in both blood cells and gills [83]. Short term exposure of a
anthropogenic sources such as metal mining, combustion of coal, high concentration of nickel resulted in stress reaction of common
oil and gasoline, battery manufacturing, lead-arsenate pesticides, carp Cyprinus carpio. Alteration of haematological parameters
lead-based paint, pigments, food cans etc., [65]. Lead discharge and behavioural changes were also found in Cyprinus carpio, to
from various industries, agricultural fields, street runoff, lead sublethal concentration of nickel exposure [84]. Nickel toxicity
dust and municipal wastewater that directly come to the aquatic showed some adverse effect on protein metabolism of freshwater
environment and cause toxicity for the aquatic life [66]. The fish, Cyprinus carpio. The observed alterations were decrease
solubility of lead in water is depending upon pH, salinity, hardness of structural, soluble and total proteins, increase of free amino
etc. Highest solubility of lead is observed in soft and acidic water. acids and protease activity and ammonia in gill and kidney after
The lethal concentration of lead for fish is 10-100 mg/L [67]. exposure to a lethal concentration of nickel [85]. Nickel poisoning
Sublethal concentration of lead exposure causes behavioural change, in fish showed loss of body equilibrium and behavioural changes
impotency and growth retardation of fish [68]. Katti reported a like surfacing, rapid mouth and operculum movement before
change in lipid and cholesterol content in the liver, brain and gonad death [86].
of Clariasbatrachus, in prolonged exposure to a low concentration Nickel accumulates in the blood, kidney, muscle and liver of
of lead nitrate [69]. Histological distortion of gill and liver tissue fish but highest accumulation is observed in the kidney [87].
was observed in African catfish Clariasgariepinus, exposed to lead. Bioaccumulation expressed a general decrease of glycogen level
Freshwater teleost (Mastacembelus pancalus) showed histological in both liver and muscle of Tilapia nilotica. High level of nickel
alterations in the ovarian tissue in lead exposure [70]. Necrosis of bioaccumulation in Tilapia nilotica, elevated blood cell count,
parenchyma cells, fibrosis of hepatic cords and connective tissue, packed cell volume and haemoglobin content and caused
reduction in growth and body weight, collapsing of blood vessels lymphopenia and leukopenia.
were also observed in lead-exposed fish [71]. Lead exposure in Nile
tilapia (Oreochromis niloticus) showed decreased haemoglobin Arsenic (As)
content, red blood cell count and hematocrit value [72]. Oxidative Arsenic is a ubiquitous element, release in the aquatic environment
stress is induced by lead toxicity, which caused synaptic damage from various anthropogenic sources including manufacturing
and neurotransmitter malfunction in fish [73]. Alteration of the companies, smelting operations, power plants etc. Another major
source of arsenic from the agricultural field is the use of arsenic our environment [102].
pesticides, herbicides and fungicides [88].
Apart from elementary form, mercury is present in an ionic form
Fish are continuously exposed to arsenic-contaminated water which forms a compound with sulphide, chloride or organic acid
through their gill and skin and also by arsenic-contaminated and organic form, especially methyl mercury [103]. Literature
food. Arsenic is present in various forms, i.e. element, trivalent suggests methyl mercury is the most chemically toxic form of mercury
and pentavalent oxidative form. Inorganic arsenic in trivalent and 70-100% of mercury present in the fish body is of methylated
oxidation state (arsenites) is very rapidly absorbed into the fish form. Methylation of inorganic mercury occurs by microorganisms
tissue and is more toxic than the pentavalent state (arsenates). such as anaerobic sulphate-reducing bacteria, iron reducers, and
The toxic effect of arsenic is dependent upon different abiotic methanogens [104,105]. Increase in water temperatures attributed
factors of a water body such as pH, temperature, salinity, organic to climate change which stimulates the methylation of mercury.
matters, phosphate content, suspended solids as well as other Mercury can enter into the fish body by food through the
toxic substances [89]. Continuous exposure of freshwater fish alimentary canal, skin and gills. The acute lethal concentration of
to the low concentration of arsenic results in bioaccumulation inorganic mercury is 0.3-1.0 mg/L for salmonids and 0.2-4 mg/L
mostly in the liver and kidney tissue [90]. Arsenic exposure showed for cyprinids depending upon the physical and chemical property of
histopathological alteration in gills and liver tissue of freshwater water. The acute lethal concentrations of commonly found organic
fish, tilapia (Oreochromis mossambicus). The alterations in gills mercury compounds are 0.025-0.125 mg/L for salmonids and 0.20-
were epithelial hyperplasis, lamellar fusion, epithelial lifting and 0.70 mg/L for cyprinids. The maximum admissible concentration
oedema, desquamation and necrosis. The liver histology showed of the inorganic form of mercury for salmonids is 0.001 mg/L and
macrophage infiltration, vascularisation, hepatocytes shrinkage, for cyprinids is 0.002 mg/L [106]. Mercury is very toxic for fish
dilation of sinusoids, vascular degeneration, nuclear hypertrophy and at sublethal concentration and causes structural, physiological
and focal necrosis [91]. A range of histological alterations was found and biochemical alteration on the fish nervous system. Methyl
in the heart of freshwater teleost, Channa punctata including mercury is considered as the most neurotoxic compound because
necrosis in the heart tissue [92]. Acute exposure of common Indian it can cross the blood-brain barrier due to its lipophilic nature and
catfish Clariasbatrachus to sodium arsenite elicited disturbed can accumulate in the nervous system of fish. Mercury can also
haemopoiesis, disruption of the erythrocyte membrane, impaired interfere with the physical property and structural integrity of cell
iron uptake by erythrocytes and haemolysis [93]. Arsenic exposure membrane by affecting the configuration of purines, pyrimidines
in the catfish Clariasbatrachus showed a time-dependent change and nucleic acids [107]. Chronic exposure of mercurial compound
in total leucocyte count and reduction of organo-somatic indices to the kidney of Clarias batrachus expressed damage and necrosis
in kidney and spleen. Arsenic also induced alteration in T-cell and of kidney tubules [108]. Mercury oxide toxicity on African catfish
B-cell functioning and interfere bacterial phagocytosis function of Clarias gariepinus showed a significant increase of serum cortical,
catfish [94]. Developmental arrest of Japanese medaka (Oryzias cholesterol, aspartate aminotransferase, alanine aminotransferase,
latipes) embryo was observed in the sublethal concentration of alkaline phosphorous, urea and creatinine levels and a significant
arsenic toxicity [95]. The induction of stress response proteins were decrease in haemoglobin and haematocrit value [109]. The
found in rainbow trout Salmo gairdnerii, on arsenic exposure [96]. freshwater fish Channa punctatus exposed to 0.3 mg/L of HgCl2
Arsenic toxicity in zebrafish embryos significantly inhibits genes for 7 days showed oxidative damage and up regulation of pro-
involved in innate immune responses, which function against viral inflammatory cytokines [110]. Inorganic mercury exposure in zebra
and bacterial infection [97]. Wanget treated two fish cell lines, JF fish showed histological alteration and oxidative stress in gonads.
(fin cells of Therapon jarbua) and TO-2 cells (ovary cells of Tilapia), Mercury toxicity also disrupted the transcription of Hypothalamic-
with sodium arsenite [98]. They observed apoptosis in JF cells Pituitary-Gonadal (HPG) axis genes and altered the sex hormone
probably due to induction of oxidative stress and distortion of the levels of adult zebra fish [111]. The male reproductive system of
cell cycle in TO-2 cells. In long term exposure of freshwater fish tropical fish Gymnotus caropo showed sensitivity to Hg toxicity.
Colisa fasciatus, to arsenic oxide caused impaired ovarian function HgCl2 induced seminiferous tubule disorganization, congestion
and reduction in the development of 2nd and 3rd stage oocyte [99]. of blood vessels, interstitial tissue proliferation, and reduction in
Bioaccumulation of arsenic affects various physiological systems of germ cells and sperm’s number of Gymnotus caropo [112].
fish such as growth, reproduction, gene expression, ion regulation,
Mercury has a high affinity to proteins, therefore more than 90%
immune system and histopathology.
of total mercury accumulates in fish muscle [113]. Rate of methyl
Mercury (Hg) mercury excretion from fish body is extremely slow therefore in
addition to muscle, high concentration of mercury also found in
Mercury is considered as one of the most toxic heavy metal
blood [114]. Additionally, liver also function as the site of storage,
found in the environment. Mercury contamination in the
detoxification or redistribution of mercury [115].
environment increased rapidly from the 20th century due to
huge industrialization [100]. Mercury ranked third in the list of Zinc (Zn)
the hazardous substance of the environment after lead and arsenic
Zinc contamination in the environment is increasing because
by United State Environmental Protection Agency (EPA) and
of different anthropogenic sources such as industrial activities,
the Agency for Toxic Substances and Disease Registry (ATSDR)
mining, combustion of coal and waste materials, steel processing
[101]. The natural sources of this element are forest fire and
etc., [116].
volcanic eruption and anthropogenic sources include fungicides,
electronic equipment, batteries, paint etc. Burning of fossil fuels Zinc is a ubiquitous trace element and one of the essential
and mining also contribute a major role in mercury pollution of micronutrients for living organisms. Zinc is involved in various
metabolic pathways such as nucleic acids and protein synthesis,
immunity, energy metabolism, cell division and body growth. It acts isoforms of MTs bound to various metals with different affinities
as a cofactor for many enzymes that aid in metabolism, digestion, in fishes [136].
nerve function and other processes [117,118]. Deficiency of zinc
causes several physiological disorders such as poor pregnancy rate,
cardiovascular diseases and cancer; but it becomes toxic in excess
amount [119]. Zinc toxicity is also species-specific and varies with
different developmental stages of fish. The toxic effect of zinc
on aquatic animals depends upon several environmental factors,
especially temperature, water hardness, and dissolved oxygen
concentration. At an acute toxic concentration of zinc, it kills fish
by destroying gill tissue and at the chronic toxic level, it induces
stress which results in the death of fish [120].
Fish take zinc through the gastrointestinal tract and gills. The
major mechanism of zinc toxicity occurs as the divalent cationic
form which disrupts the absorption of calcium ion in the tissue,
results in hypocalcaemia and eventually fish death [121]. Zinc Figure 1: Heavy metals toxicity in fishes. Heavy metals induce oxidative
sulphate exposed Tilapia nilotica showed slow swimming activity stress by generating reactive oxygen species (ROS). The anti-oxidation
and loss of body equilibrium. The hepatocytes of the liver became defense mechanism (include different enzymes CAT, SOD, GST, GPx
vacuolated with frequent necrosis [122]. Zebrafish embryos and metal scavenging protein MT) involved in detoxification. Severe
exposed to different concentrations of ZnCl2 showed a delay in metal toxicity generates different physiological and immunological
hatching capacity, growth defect and skeletal malformations due to responses. In the course of metal toxicity bioaccumulation of metals
defective calcification [123]. Zinc exposed fish Phoxinus phoxinus occurs in different tissue of fishes.
showed alteration in movement pattern and behavioural change.
These fish become less active, easily frightened and formed denser In addition, to detoxify the metals, metallothioneins are the major
shoals which mostly stayed close to the bottom [124]. Zinc exposed cause of bioaccumulation of heavy metals in different tissue of
killifish (Fundulus heteroclitus) led to oxidative stress response by fishes [137]. The accumulated heavy metals not only affect the
increasing hepatic lipid peroxidation level, which is an oxidative fish population in the aquatic ecosystem but also transfer through
stress biomarker and decrease of liver catalase (CAT) activity [125]. the food chain/web to the next tropic level. Trophic transfer of
these elements from aquatic to the terrestrial ecosystem has serious
Zinc accumulates in fish through gills and digestive track, however implications for human health by promoting different diseases
the role of water as a source of zinc is not fully elucidated [126]. including cancer, neurodegenerative disease, etc. [138,139].
Murugan examined the accumulation of zinc in different tissue of
Channa punctatus and concluded that zinc deposit at the order of
liver>kidney> intestine>gill>muscle [127]. Therefore, this comprehensive study about the heavy metal toxicity
CONCLUSION on fish health suggests that essential steps should be taken to
minimize the toxic impact of heavy metals on human health and
Some heavy metals have an essential role in the normal biological the environment. Here, some recommendation is made-
processes, and the insufficiency or excess amount can cause a
disturbance in the metabolic pathways and serious illness [128]. • The level of heavy metal on soil, water and sediment should
Essential heavy metals are which have known biological functions be monitored regularly. Such data should be used for the
(Table 2) [129]. Other group of heavy metals have no biological assessment of health risk in the human population.
role and at higher concentrations cause a toxic effect to the tissues • Agricultural and industrial waste should be decontaminated
[130]. effectively before discharge into the water body.
Beyond tolerance level, metal ions induce Reactive Oxygen Species • Proper awareness should be provided to the public about the
(ROS) production, which causes an oxidative stress response harmful effect of heavy metal toxicity in our environment.
in fishes [131]. Redox-active metals e.g. copper and chromium
• More scientific research should be encouraged and promoted
generate reactive oxygen species through redox cycling. Whereas
about the toxicity of heavy metals, their trophic level transfer
redox inactive metals e.g. mercury, nickel, lead, arsenic and
and their effect on the environment.
cadmium bind to the Sulfhydryl groups (SH) of proteins involved
in antioxidant defences, thereby impair the defence mechanism AUTHOR CONTRIBUTION
[132]. Elevated ROS production in fish causes DNA lesions,
oxidation of lipids and proteins and alterations of cellular redox Pramita Garai, Priyajit Banerjee are contributed equally.
status [133,134].
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