The neurological toxicity of heavy metals: A fish perspective

Green, Adrian; Planchart, Antonio

doi:10.1016/j.cbpc.2017.11.008

Cited by 87 publications

(42 citation statements)

References 120 publications

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“…Casein 1 27.0 Fish meal 2 32.0 Wheat flour 3 18.0 Dextrin 1 4.20 Corn starch 2 3.50 Fish oil 4 6.10 Vitamin premix 5 3.00 Mineral premix 6 3.00 Cellulose 1 3.20 Hg-premix (5000 ppm) 0.00…”

Section: Ingredients % In Dietmentioning

confidence: 99%

“…All forms of mercury are toxic [4], and organic MeHg is neurotoxic compared to inorganic HgCl 2 in fish [5]. Although mercury is a naturally occurring element, human or anthropogenic activities, particularly through industrial processes, have led to widespread distribution of toxic mercurial derivatives throughout the biosphere [6]. In aquatic conditions, the natural mercury is biologically transformed into organic mercury by different types of microorganisms, basically anaerobic bacteria [7].…”

Section: Introductionmentioning

confidence: 99%

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Evaluation of Dietary Organic and Inorganic Mercury Threshold Levels on Induced Mercury Toxicity in a Marine Fish Model

Raihan

Moniruzzaman

Park

et al. 2020

Animals

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Mercury as one of the most toxic elements can be present in organic or inorganic form in marine fishes, which may cause a potential threat to public health. In this study, we investigated to determine the dietary organic (O-Hg) and inorganic (I-Hg) mercury threshold levels on induced mercury toxicity in juvenile olive flounder, Paralichthys olivaceus as a marine fish model. Twenty-eight fish averaging 3.1 ± 0.05 g (mean ± SD) were arbitrarily assigned to each of 27 tanks. Each tank was arbitrarily restricted to triplicates of nine experimental diets for eight weeks. The experimental diets were manufactured to contain 0 (Control), 10 (I-Hg10, O-Hg10), 20 (I-Hg20, O-Hg20), 40 (I-Hg40, O-Hg40) and 160 (I-Hg160, O-Hg160) mg/kg diet in organic form as methylmercury (MeHg) or in inorganic form as mercuric chloride (HgCl2). At the termination of the experimental trial, weight gains (WGs) of fish fed the control and 10 (I-Hg10, O-Hg10) diets were remarkably higher than those of fish fed the 20 (I-Hg20, O-Hg20), 40 (I-Hg40, O-Hg40) and 160 (I-Hg160, O-Hg160) (p < 0.05). Specific growth rate and feed efficiency of fish fed control and 10 (I-Hg10, O-Hg10) diets were significantly higher than those of fish fed 40 (I-Hg40, O-Hg40) and 160 (I-Hg160, O-Hg160) diets. In comparison to the dietary inorganic mercury, dietary MeHg bioaccumulation rates were significantly higher in the tissue levels according to the dietary inclusion levels. MeHg accumulated mostly in kidney, followed by liver and gill tissues. HgCl2 accumulated in tissues, in decreasing order, liver > kidney > gills. A broken-line regression model for percentage of WG indicated that the threshold toxicity level for an Hg-incorporated diet of juvenile olive flounder could be 13.5 mg Hg/kg in the form of HgCl2 and 8.7 mg Hg/kg in the form of MeHg.

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“…Casein 1 27.0 Fish meal 2 32.0 Wheat flour 3 18.0 Dextrin 1 4.20 Corn starch 2 3.50 Fish oil 4 6.10 Vitamin premix 5 3.00 Mineral premix 6 3.00 Cellulose 1 3.20 Hg-premix (5000 ppm) 0.00…”

Section: Ingredients % In Dietmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Evaluation of Dietary Organic and Inorganic Mercury Threshold Levels on Induced Mercury Toxicity in a Marine Fish Model

Raihan

Moniruzzaman

Park

et al. 2020

Animals

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“…Heavy metals can accumulate in various organs, including the liver, heart, kidney, and brain, and greatly affect their function. In the last few decades, the presence of neurological damage following acute and chronic exposure to heavy metals has been increasingly evident [90,91]. In particular, it has been shown that the accumulation of some metals can alter the process of myelination, possibly leading to neurodegeneration [92,93].…”

Section: Intake Of Heavy Metals and Oligodendrocytesmentioning

confidence: 99%

Environmental and Nutritional “Stressors” and Oligodendrocyte Dysfunction: Role of Mitochondrial and Endoplasmatic Reticulum Impairment

et al. 2020

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Oligodendrocytes are myelinating cells of the central nervous system which are generated by progenitor oligodendrocytes as a result of maturation processes. The main function of mature oligodendrocytes is to produce myelin, a lipid-rich multi-lamellar membrane that wraps tightly around neuronal axons, insulating them and facilitating nerve conduction through saltatory propagation. The myelination process requires the consumption a large amount of energy and a high metabolic turnover. Mitochondria are essential organelles which regulate many cellular functions, including energy production through oxidative phosphorylation. Any mitochondrial dysfunction impacts cellular metabolism and negatively affects the health of the organism. If the functioning of the mitochondria is unbalanced, the myelination process is impaired. When myelination has finished, oligodendrocyte will have synthesized about 40% of the total lipids present in the brain. Since lipid synthesis occurs in the cellular endoplasmic reticulum, the dysfunction of this organelle can lead to partial or deficient myelination, triggering numerous neurodegenerative diseases. In this review, the induced malfunction of oligodendrocytes by harmful exogenous stimuli has been outlined. In particular, the effects of alcohol consumption and heavy metal intake are discussed. Furthermore, the response of the oligodendrocyte to excessive mitochondrial oxidative stress and to the altered regulation of the functioning of the endoplasmic reticulum will be explored.

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“…In fact, it affects almost all tissues and organ systems, such as the respiratory, hematopoietic, renal, cardiovascular, urinary, and urogenital systems, as well as bones [ 2 , 3 , 4 , 5 ]. Moreover, apart from its widely characterized effects in humans [ 4 , 5 , 6 , 7 , 8 ] and animals [ 3 ], the detrimental effects of Pb on the physiology of plants [ 9 ] and fish [ 10 , 11 , 12 ] have also been well-documented.…”

Section: Introductionmentioning

confidence: 99%

(Ascorb)ing Pb Neurotoxicity in the Developing Brain

Ahmad

Liu

2020

Antioxidants

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Lead (Pb) neurotoxicity is a major concern, particularly in children. Developmental exposure to Pb can alter neurodevelopmental trajectory and has permanent neuropathological consequences, including an increased vulnerability to further stressors. Ascorbic acid is among most researched antioxidant nutrients and has a special role in maintaining redox homeostasis in physiological and physio-pathological brain states. Furthermore, because of its capacity to chelate metal ions, ascorbic acid may particularly serve as a potent therapeutic agent in Pb poisoning. The present review first discusses the major consequences of Pb exposure in children and then proceeds to present evidence from human and animal studies for ascorbic acid as an efficient ameliorative supplemental nutrient in Pb poisoning, with a particular focus on developmental Pb neurotoxicity. In doing so, it is hoped that there is a revitalization for further research on understanding the brain functions of this essential, safe, and readily available vitamin in physiological states, as well to justify and establish it as an effective neuroprotective and modulatory factor in the pathologies of the nervous system, including developmental neuropathologies.

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The neurological toxicity of heavy metals: A fish perspective

Cited by 87 publications

References 120 publications

Evaluation of Dietary Organic and Inorganic Mercury Threshold Levels on Induced Mercury Toxicity in a Marine Fish Model

Evaluation of Dietary Organic and Inorganic Mercury Threshold Levels on Induced Mercury Toxicity in a Marine Fish Model

Environmental and Nutritional “Stressors” and Oligodendrocyte Dysfunction: Role of Mitochondrial and Endoplasmatic Reticulum Impairment

(Ascorb)ing Pb Neurotoxicity in the Developing Brain

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