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Toxic Metal Removal Using Microbial Nanotechnology
Published in Mahendra Rai, Patrycja Golińska, Microbial Nanotechnology, 2020
Although Cu is an essential element, its level in the body largely varies with food intake. Higher levels of Cu are often observed due to consumption of Cu-rich foods like oysters, liver, nuts, legumes, whole grains, and dried fruit (Shokunbi et al. 2019). Windblown dust, volcanoes, and forest fires, Cu smelters, iron and steel production industries, and municipal incinerators release Cu into the air (Cai et al. 2019). Cu is bound to amino acids like histidine, methionine, and cysteine that facilitate its absorption through an amino acid transport system. Cu forms ligands with reduced glutathione, citric, gluconic, lactic, and acetic acids that are readily absorbed. Other sources of Cu include machinery, construction, transportation, military weapons, and jewellery. Dental products, intrauterine devices and cosmetics also use Cu (Gutiérrez et al. 2019). Elevated levels of Cu are associated with hepatotoxicity, liver cirrhosis, and hemolysis and lead to damage of renal tubules, brain, and other organs. Severe patho-physiological conditions may result in coma, hepatic necrosis, vascular collapse, and death. Cu-contaminated water or foods may result in Cu poisoning indicated by weakness, lethargy, anorexia, erosion of epithelial lining of the gastrointestinal tract, hepatocellular necrosis in the liver, acute tubular necrosis in the kidney, obstructive bile excretion, primary biliary cirrhosis, obstructive hepatobiliary disease, extrahepatic biliary atresia, neonatal hepatitis, choledochal cysts and α-1-antitrypsin deficiency (Gaetke and Chow 2003).
Metals, Metal Oxides, and Their Composites—Safety and Health Awareness
Published in Vijay B. Pawade, Paresh H. Salame, Bharat A. Bhanvase, Multifunctional Nanostructured Metal Oxides for Energy Harvesting and Storage Devices, 2020
There is a report wherein a 38-year old healthy man was exposed to nickel sprayed in an arc process. He lost his life after 13 days of exposure, and the reason for death was attributed to respiratory disease syndrome. Ni NPs of size <25 nm were found in lung macrophage on examination with TEM. Moreover, a higher concentration of Ni was observed in the urine, meaning that inhaled NPs can journey systemically and influence the kidneys and therefore develop an acute tubular necrosis, implying that the kidney is vulnerable to damage. Furthermore, in regard to health risk evaluation in humans, a World Health Organization (WHO) reports that nickel salts in general, irrespective of their size, are carcinogens via inhalation exposure, and since there is a linear dose response, there are no safety limits as such for nickel compounds worth recommending. The concentrations responsible for an excessive lifetime risk potential of cancer are of the order of 0.25 and 0.025 μg/m3, respectively.
Pesticides and Chronic Diseases
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Trivalent arsenicals (or, more likely an arsenious acid metabolite) bind efficiently to the functional thiol groups of many tissue components, including enzymes. Its affinity for thiol groups in keratin accounts for the accumulation of arsenic in skin, nails, and hair in cases of chronic poisoning. When absorbed across the gut wall, these arsenicals injure the splanchnic vasculature, causing abdominal pain, colic, and diarrhea. Once absorbed into the blood, they cause toxic damage to the liver, kidneys, brain, bone marrow (BM), and peripheral nerves. Liver injury is manifest as hepatomegaly, jaundice, and an increase in circulating hepatocellular enzymes LDH and GOT. Renal damage is reflected in albuminuria, hematuria, pyuria, cylinduria, and then azotemia. Acute tubular necrosis may occur in severe poisoning. Injury to blood-forming tissues can take the form of agranulocytosis, aplastic anemia, thrombocytopenia, or pancytopenia. Toxic encephalopathy may manifest as speech and behavioral disturbances. Peripheral neuropathy occurs in both acute and chronic forms.
Hemolysis during short-term mechanical circulatory support: from pathophysiology to diagnosis and treatment
Published in Expert Review of Medical Devices, 2022
Tim Balthazar, Johan Bennett, Tom Adriaenssens
Hemolysis can lead to a self-perpetuating cycle of multi-organ thrombosis and injury (as shown in Figure 2). The mediators released by destructed RBC’s exert pro-thrombotic effects. Plasma-free hemoglobin (pfHb) plays a crucial role; it scavenges circulating nitric oxide (NO) and reduces von Willebrand factor degradation [26]. Also, arginase from the RBC consumes L-arginine, which is needed for endothelial NO production [28]. This leads to vasoconstriction and reduced NO-mediated platelet inhibition. In addition, small-membrane vesicles, carbon monoxide as well as iron are released in the circulation to exert pro-thrombotic effects and further stimulate the negative spiral of thrombosis, vasoconstriction, and ischemia-reperfusion [26,28]. Locally in the kidney, the accumulation of large amounts of hemoglobin derivatives (heme, heme proteins, and hemosiderin) in the cells of the proximal tubule can lead to acute tubular necrosis (ATN) because of direct cytotoxicity, endothelial dysfunction, and renal vasoconstriction [29,30]. Moreover, the formation of methemoglobin casts in the distal tubule may cause intrarenal obstruction, eventually worsening the injury to the proximal part of the tubule. These mechanisms explain how the kidney is often the first organ to suffer from failure in the case of severe intravascular hemolysis [29,30]
Adsorption performance of activated carbon synthesis by ZnCl2, KOH, H3PO4 with different activation temperatures from mixed fruit seeds
Published in Environmental Technology, 2022
As a result of the advancement of nuclear energy, mining and chemical production, high levels of toxic heavy metal ions are released into the environment, creating grave dangers to underground and surface mediums [1–3]. The continuous exposure to heavy metal ions, high toxicity and accumulation in living organisms can cause the long-time health problems in humans and other types [4–6]. Therefore, it is essential to remove the heavy metal ions from the polluted water [7,8]. Water pollution is one of the most significant subjects to protect the environment. For human and living organisms, heavy metals such as Cr(III), Cd(II), As(III), Cu(II), Zn(II), Ni(II), Pb(II), are toxic and health hazards if their concentrations exceed the permissible limits [9,10]. The long-time exposure to toxic metals causes human health problems such as carcinoma, anaemia, liver and kidney injury. Nickel is a toxic metal and is known to be carcinogenic. According to the World Health Organization (WHO), Ni(II)and Cu(II) concentrations in aqueous solutions should be below 0.2 and 2 mg/L, respectively [11]. A high intake of copper into the human body can oxidize DNA, lipids and proteins inside the cell. Therefore, it can potentially cause cancer [12]. Oral exposure to Cr(III) in humans is due to contaminated water. Exposure to chrome causes indigestion, kidney failure mouth ulcers, abdominal pain, acute tubular necrosis, vomiting, and lung cancer [13]. For this reason, the toxic heavy metals should be taken from the water to keep human health and the perimeter [14].
Carnosine in health and disease
Published in European Journal of Sport Science, 2019
Guilherme Giannini Artioli, Craig Sale, Rebecca Louise Jones
Acute kidney failure is defined as a sudden, sustained impairment of kidney function, typically for periods of 1–7 days, resulting in reduced glomerular filtration rate, urinary volume, electrolyte imbalance and impaired pH regulation. Kidney damage induced by ischemia/reperfusion is a key factor involved in the pathogenesis of acute kidney failure and it is commonly observed in various clinical conditions, such as recovery from cardiac arrest, kidney transplantation and partial nephrectomy (Thadhani, Pascual, & Bonventre, 1996). Acute kidney failure may also result in acute tubular necrosis and increased renal vascular resistance (Thadhani et al., 1996), thereby being typically accompanied by impaired renal blood flow (Basile, Anderson, & Sutton, 2012). Although the molecular mechanisms underpinning these responses are not fully elucidated, ATP depletion, oxidative damage, phospholipase activation, neutrophil infiltration and exacerbation of adrenergic activation have been shown to play a central role in the pathogenesis of acute kidney failure (Basile et al., 2012). Any substance capable of suppressing or attenuating any of the processes involved in its pathogenesis may, therefore, be protective during episodes of acute failure (Fujii et al., 2003), thus reducing the area of the kidney where cells suffer lethal injuries. Reducing lethal injuries to the point of non-lethality is critical for recovery and regeneration (Basile et al., 2012).