Biological and Clinical Sciences Research Journal
ISSN: 2708-2261
www.bcsrj.com
DOI: https://doi.org/10.47264/bcsrj0101045
Biol. Clin. Sci. Res. J.,
Volume, 2020: e045
Mini Review Article
TOXIC EFFECTS OF LEAD ON FISH AND HUMAN
ISHAQUE
A1*, ISHAQUE S, ARIF A1, ABBAS HG2
1Institute of Molecular Biology and Biotechnology, The
University of Lahore, Lahore, Pakistan
2Department of Biotechnology, Kinnaird College for Women, Lahore, Pakistan
3Cotton Research Institute, Ayub Agricultural
Research Institute Faisalabad, Pakistan
Corresponding author: asmaishaque137@gmail.com
Abstract
Bioaccumulation
is a characteristic aspect in toxicity caused by Pb
exposure. Toxic effects are induced in fish due to Pb
exposure effecting its biochemical and physiological functions. Exposure
pathway (dietary and waterborne), environmental factors (salt-water or fresh
water) and Pb binding capacity with protein, SH and
sulfur group decide accumulation pattern of Pb
exposure. Activation of antioxidant responses like TBARS, GSH, GST, CAT and SOD
occurs in fish for its protection in response to the oxidative stresses induced
in fish due to Pb accumulation. Disruption of neurotransmitter
function also occurs due to Pb accumulation which
causes neurotoxicity in fish. Pb interaction also
disturbs immune system responses. In fish, various systems are affected due to Pb toxic exposure which can be used as an indicator of
toxicity in aquatic environment.
Keywords:
Lead, heavy metal, toxicity, antioxidant,
biochemical, physiological
Earth
crust contains lead in trace amount that is generally found in plant, rocks,
air, water and soil (Cheng and Hu, 2010). Although aquatic habitats are
omnipresent with lead but anthropogenic activities that include smelting,
mining, manufacturing of paints, cement and batteries raise its level (Chain, 2010; Flegal, 1986; Kim and Kang, 2016b). Lead combines
(naturally) with other elements to form lead compounds and in environment it occurs
predominantly in inorganic form (Pb II, TEL, trimethyl lead), however organic states found which was reported
record toxic in the form of TtEL (Chang et al., 2007; Chen et al., 2014; Flegal, 1986;
Lee and Jiang, 2005). Pb bio- magnification does not occur in food chain.
Accumulation of pb in older
organisms causes the increase in body burden as they are stored on bony
tissues.
Lead
compound mainly target reproductive (Apostoli et al., 1998; Assennato et al., 1987;
Braunstein et al., 1978; Lerda, 1992; Telisman et al., 2000), digestive (Sakai, 2000), skeletal (Oflaherty, 1995), peripheral and central NS (Campara et al., 1984; Hogstedt et al., 1983; Lead,
1995; Mantere et al., 1984), immunological
system (Coscia et al., 1987; Ewers et al., 1982; Gidlow,
2015) and kidney (Ehrlich et al., 1998; Gerhardsson et al., 1992;
Goyer, 1989; Lead, 1995; Loghman-Adham, 1997). While chronic Pb
exposure leads cardiotoxicity (Evis et al., 1987; Lai et al., 1991), neurotoxicity, nephrotoxicity (Khalil-Manesh et al., 1993), carcinogenicity (IARC, 2006) and genotoxicity
(IARC, 2006) in humans. Ingesting Pb contaminated sea food causes acute toxicity in kidney
and brain. Pb gastrointestinal absorption is
dependent on iron, calcium status of the human body as well on the age that is kids
are more vulnerable as they absorb more lead. Lead is accumulated in bones,
blood and soft tissue after its absorbance into the blood steam.
Lead has high affinity with protein due
to its stable complex formation with sulfur and oxygen atom of protein structure
(Verstraeten et al., 2008). Ferrochelatase
(involve in the catalyzation of porphyrin
ring by iron), delta-aminolevulinic acid synthase (synthesize porphobilinogen
(PBG) which is important for biosynthesis of hemeproteins)
and delta-aminolevulinic acid dehydratase
are three vital human heme enzymes which are
inhibited due to Pb accumulation. This inhibition
causes hemoglobin level to drop and inhibit the metabolism of cytochrome P450- dependent phase (Alvares et al., 1976; Bernard and Lauwerys, 1984;
Goering, 1993; Jaishankar et al., 2014; Philip and Gerson, 1994; Ponka, 1999).
Inhibition of inocytes basolateral transport mechanism in the epithelium of gills
causes hypocalcemia in fish due to lead accumulation.
It is because of lead high affinity with Ca2+ ATPase,
Na2+K+ ATPase and Na+Ca2+
exchanger which disturb ion regulation and electrochemical gradient in cells (Verstraeten et al., 2008).
Hence, bioaccumulation even at small concentration due to Pb
exposure can prove fatal to aquatic animals (Kim and Kang, 2015b). Lead poisoning
and oxidative stress can be caused by the imbalance between antioxidants and
pro oxidants (Kim and Kang, 2017b). In fish,
persuaded intensified antioxidant response due to lead exposure can produce ROS
(reactive oxygen species). Pb has high affinity for
RBCs which result in toxic effects on function and structure of cellular
membranes and cause high oxidative stress in fish (Gurer and Ercal, 2000).
Immunological parameter including piscine immune system is being affected due
to the lead stress (Kim and Kang, 2016c).
In animals, Pb acts as a critical immune toxicant (Paul et al., 2014).
Lead has diverse stroke exposure and toxic effects; thus, an inclusive research
is needed to define the Pb exposure in fish.
Metals
show its toxic effects in fish when they are taken up by the body and is bioaccumulated followed by the detoxification mechanism,
metabolic and excretory process (Eroglu et al., 2015). In fish metal contamination
occur either through gastrointestinal track when they intake contaminated food
or through gill if metal ions are present in water. Liver as metal excretory
system play its role in binding of Pb to steroid in
bile and then out of the body through feces (Sures et al., 2003; Zhai et al., 2017). Circulatory system is
responsible for circulating the ingested metal to rest of body (Zhai et al., 2017), where metals either stored in
tissues, or is lethal to target organ or is excreted outside the body via gills
and kidney (Kim and Kang, 2014, 2015a, 2016a). Dietary
exposure of Pb to juvenile rockfish, Sebastes schlegelii,
show accumulation of Pb in its various tissue include gills, intestine, liver and spleen. Hwang et
al. (2016) also testified the similar trend of Pb
accumulation in Platichthys stellatus who was experienced to dietary Pb.
Ca2+,
Na+ and K+ ionic homeostasis is disturbed when body have
chronic exposure against lead (Grosell et al., 2006). Antagonistic actions of Ca2+
and Pb2+ lessen Pb toxicity in fish body
because Ca2+ stick to dissolved ambient Pb and help
to lower Pb accumulation in body (Alves et al., 2006; Audesirk, 1993; Rogers et al.,
2003). There are two
pathways by which metal can accumulate in the body i.e. dietary or waterborne
metal exposure. Water borne exposure
result in the accumulation of metal in gills because during osmoregulation
and respiration, gills come in direct contact with metal (Alves et al., 2006; Rogers et al., 2003). While dietary exposure
accumulates high metal concentration in intestinal tissues (Alves et al., 2006; Castro-González and
Méndez-Armenta, 2008). Water borne exposure has high
risk of Pb accumulation in the gills as compared to
the dietary intake (Dural et al., 2007; Farkas et al., 2003; Grosell et
al., 2006; Kalay et al., 1999; Souid et al., 2015). Metals bound
to the subcellular fractions of prey when the gut is
exposed to dietary metal pathway makes the microbiota
to reduce however when exposed to water the bioavailability is 20-60 times more
(Alsop et al., 2016). Environmental differences also
play its role in the bioaccumulation of the metal i.e. sea water and fresh
water. To avoid from dehydration under high osmotic pressure condition, marine
fish drink a lot of water that cause prominent metal accumulation in the
intestinal tissue. While in the case of fresh water specie, gills are at high
risk of metal accumulation because fish under low osmotic pressure environment
actively transport ions outside the body through inocytes
in the gill (Kim and Kang, 2014). Metabolic active organs have
been reported to be on a high risk for metal accumulation. Acute or chronic Pb effects the target organs liver and kidney, due to their
role in detoxification and elimination of toxic element outside the body (Javed, 2012; Patra et al., 2001; Vinodhini and
Narayanan, 2008; Zhai et al., 2017). Spleen is
also accumulated with Pb because it functions in the
removal of xenobiotic from blood (Kim and Kang, 2015b; Somero et al., 1977). Gills and intestine accumulate
Pb directly from water or food (Kim and Kang, 2017a). Pb accumulation has
been reported lowest in the fish muscles and it is important indicator of food
safety because fish muscles are directly accumulated by the humans (Al-Balawi et al., 2013; Dural et al., 2007; Farkas et
al., 2003; Sures and Siddall, 1999; Zhai et al., 2017).
Pb is neuro toxicant whose exposure
directly affect CNS of fish that results in the neurotoxicity, cognitive and
behavioral dysfunction (Hsu and Guo, 2002; Zhu et al., 2016). Pb neurotoxicity
causes neurogenerative disorder, neurotransmission
impairment and cell signaling deregulation and change in brain morphology because
Pb disturb Ca2+ flux that result in
disrupting calcium regulatory functions, thus cell necrosis and oxidative
stress occurs (Marchetti, 2003; Verstraeten et al., 2008). Calcium is an important ion
for the regulation and release of neurotransmitters. Pb
makes its way into the transport system of calcium by mimicking it, and
ultimately enters the nervous system. Calcium homeostasis is disturbed due to pb accumulation and it effects the mechanisms of
neurotransmission (Westerink and Vijverberg, 2002). Brain transcription factors
are regulated by zinc finger proteins. When the body is exposed to pb, it replaces zinc ions, which result in neurological
injuries tracked by hyperactive movement that cause hyperventilation in fish (Zizza et al., 2013). Cholinesterase is an enzyme
responsible for functioning of NS by catabolizing
acetylcholine. Pb inhibits cholinesterase activity by
occupying its position that result in the accumulation of Ach which lead to
severe neurotoxicity that can be life threatening (Nunes et al., 2014). In fish, lead exposure leads
to neurotransmitter changes and synaptic damage which leads to behavioral and
neurological problems and it was observed that changes in neurotransmitter
systems were directly related to ATP (Senger et al., 2006). Pb
toxicity also damage structural and functional conformation of protein, that
alter gene expression and disturb DNA repairing process (Richetti et al., 2011). To assess the toxicity caused
by Pb in fish, neurotoxicity can be used as a
biomarker for indicating the Pb interaction to that
fish.
In
fish Pb exposure cause alteration in immune response
that effect immune functions and cause neurological disorder, physiological and
biochemical disturbance (Paul et al., 2014; Small, 2004). Environmental immune toxicant Pb also disrupt antibody production, hematopoietic and phagocytic activity also reduced (Dunier, 1996). It has been reported by (Adeyemo et al., 2010) that Pb
exposure cause tissue injury in fish, that cause change in the lymphocytes
count, Witeska (2005) reported that this decrease is
due to stress reaction which induces cortisol
secretion that promote apoptosis (Witeska, 2005). Pb
activity also disturbs cytokines expression which is responsible for regulating
immune response. In crucian carp (Dai et al., 2018) observed that Pb cause serious damage to immune system of fish as amplification
in mRNA expression of TNF and IL10 was spotted, however both factors are
responsible for inflammatory immune action and apoptosis (Dai et al., 2018; Savan and Sakai, 2006). Pb
has a toxic effect on fish immune system as it disturbs immune responses i.e.
inflammation or apoptosis of leukocytes and lymphocytes, disrupt intracellular
transduction signals by inhibiting biomolecules
activity. Thus, to determine toxicity in fish disturbed immune response is
giving the signal of Pb exposure in the environment.
Reactive
oxygen species (ROS) like superoxide radicals, hydroxyl radicals and hydrogen
peroxides are produced in fish due to the induction of oxidative stress when
metal gets accumulated in its tissues (Eroglu et al.,
2015; Kim and Kang, 2016d; Kim et al., 2017a). A Fenton reaction also occurs
due to oxidative stress which converts hydrogen peroxide to hydroxyl radicals
which causes nucleic acid and protein damage and lipid peroxidation
in fish body (Kim and Kang,2015b, c; Kim et al., 2017a). An imbalance between
biological detoxification systems (e.g., antioxidant responses like GST, GSH,
CAT and SOD) and free radicals generated causes oxidative stress in fish (Kim
and Kang, 2015c; Kim et al., 2017b). Therefore, oxidative stress in
metal-exposed-fish can be evaluated by checking for their antioxidant
responses. Superoxide dismutase (SOD) activity is directly related to the exposure
concentration of Pb i.e. SOD activity decreases as antioxidants
production decreases and SOD activity increases as ROS production as a
defensive mechanism increases (Alsop et al., 2016; Chen et al., 2014; Kim et
al., 2017a). After Pb exposure, Atli
and Canli (2007) observed amplified CAT activity in Oreochromis niloticu as
a measure to shield the tissue and cell against injury caused by ROS
generation.
The authors declared absence of conflict of interest.
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