The quest for wellness: Public health and environmental concerns
Lois N. Magner, Oliver J. Kim in A History of Medicine, 2017
During World War I, Hamilton conducted studies of war-related industries, especially factories making munitions and explosives, to establish rules for protecting workers. American factories, with little or no experience, were producing huge quantities of chemicals needed for weapons and explosives, such as dinitrobenzol, trinitrotoluol, military guncotton, fulminate of mercury, nitric acid, aniline, and rubber. Previously, America had imported many of these chemicals from Germany. In 1923, Hamilton began to study factories that produced and used mercury, one of the oldest industrial poisons. During World War I there was great demand for mercury fulminate for the detonators of high explosives. Miners were poisoned because of their exposure to mercury fumes and dust particles. Their wives were poisoned by washing clothes that were heavily contaminated with mercury. Symptoms of mercury poisoning include swelling and pain in the gums and lips, twitching limbs, tremors of the hands, fatigue, anxiety, depression, irritability, and a neurological disorder known as Mad Hatter Disease (erethism mercurialis).
Mercuric chloride and syphilis
Dinesh Kumar Jain in Homeopathy, 2022
“The metal acts in extremely low concentration if allowed sufficient time. Mercuric chloride kills B. Typhosus at dilution of 1 in 1000000 in 24 hours and at a dilution of 1 in 20000 in 22 minutes” (Wilson et al., 1975, p. 550). “Mercury was the first drug effective in treatment of syphilis” (Wilson et al., 1975, p. 234). “Like other mercury salts mercuric chloride has a specific toxic action against Treponema pallidum and has been used in treatment of syphilis” (Wilson et al., 1975, p. 234). Mercury is highly toxic to the body, 1–5 μg/ml concentration of mercury in blood produces various toxic manifestations. Acute mercury poisoning is characterized by ashen gray appearance of the mouth, pharynx, and gastric mucosa, vomiting, diarrhea, emphysema, hemorrhage. Kidney, colon, and month are also affected. Renal lesions are also produced. In chronic mercury poisoning, features are paresthesias, ataxia, visual defects, dysarthria, hearing defects, tremors, and various neurological and psychiatric symptoms. Irritability, erethism, insomnia, confusion, and forgetfulness are common psychiatric symptoms of chronic mercury poisoning. Nephrotoxicity, gingivitis, stomatitis, and other nonspecific symptoms such as anorexia, weight loss, anemia, and weakness are also associated with chronic mercury poisoning (Klaassen, 1980, pp. 1623–1625).
Inorganic Chemical Pollutants
William J. Rea, Kalpana D. Patel in Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
Both the aforementioned neurotoxicity and a human disease response to mercury exposure have been shown to be dependent on reaching a critical threshold concentration.501 Therefore, in cases of acute mercury poisoning, the direct neurotoxic effect of mercury in the brain may surpass this threshold and elicit a disease response. However, in cases of chronic mercury exposure, mercury concentrations in the brain may remain beneath the critical threshold concentration and therefore a direct relationship between chronic mercury exposure and neurotoxicity is not evident, prima facie. In toxicological studies of chronic mercury exposure in primates, organic mercury has been shown to demethylate and form inorganic mercury deposits which persist in the brain for years.495
Flavonoids fractions of Adansonia digitata L. fruits protects adult Wistar rats from mercury chloride-induced hepatorenal toxicity: histopathological and biochemical studies
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Wusa Makena, Yomi Samson Aribiyun, Aisha Aminu, Barka Ishaku, Ayuba Yohana, Ekwere Eke Inemesit
Heavy metals pollute the environment and are toxic to living organisms, and in their various forms, they exhibit distinct biological behavior, pharmacokinetics, and clinical manifestations [1–3]. It is commonly found in the environment and is linked to severe health issues in mammals, and exposure to mercury chloride (HgCl2) is via products like batteries, pesticides, and paints [1,4,5]. Mercury poisoning affects the nervous system, liver, kidney, and digestive system [6]. It is primarily metabolized in the liver before accumulating in the kidneys. As a result, the liver and kidneys are the organs most affected [7]. Mercury chloride poisoning has previously been shown to occur via several routes, including inhalation, ingestion, and skin absorption [8]. Mercury chloride also degrades antioxidants and reduces free radical scavenging systems like superoxide dismutase (SOD), Catalase (CAT) and reduced glutathione (GSH) [9–11]. The occurrence of lipid peroxidation is among the critical pathological factors in the sequence of events that leads to the onset of degenerative diseases due to disruptions in redox and calcium homeostasis [12,13].
Endoplasmic reticulum stress participates in the pathophysiology of mercury-caused acute kidney injury
Published in Renal Failure, 2019
Plácido Rojas-Franco, Margarita Franco-Colín, Alejandra Paola Torres-Manzo, Vanessa Blas-Valdivia, María del Rocio Thompson-Bonilla, Sinan Kandir, Edgar Cano-Europa
Also, some reports link mercury poisoning with organelle dysfunction, such as mitochondria, cytoskeleton, and endoplasmic reticulum, both in vivo and in vitro [7–10]. However, concerning the endoplasmic reticulum, a pathway that correlates this organelle with AKI caused by mercury has not been described. Still, some reports show that mercury and other heavy metals can interfere with proper protein folding in the endoplasmic reticulum, which can be a significant detriment to cell survival [11]. Unfolded or misfolded protein accumulation is associated with several cellular stressors, such as redox environment disturbance, a Ca2+ imbalance, altered protein glycosylation, or protein folding defects; it is known as endoplasmic reticulum stress (ERS) [12]. Meanwhile, the unfolded protein response (UPR) is a process that seeks to restore the endoplasmic reticulum’s normal function through multiple strategies mediated by the initial activation of ER membrane-associated sensors, PKR-like ER-kinase (PERK), activating transcription factor 6 (ATF6), and the inositol-requiring enzyme-1alpha (IRE1α). When the UPR is not enough to restore the organelle homeostasis, the cells activate cell-death mechanisms that are primarily mediated by the action of the UPR protein growth arrest, the deoxyribonucleic acid damage-inducible gene 153 (GADD-153, also known as CHOP), and ER membrane-associated caspase 12 [12,13].
Rethinking mercury: the role of selenium in the pathophysiology of mercury toxicity
Published in Clinical Toxicology, 2018
The role of selenium in mercury poisoning is multifaceted, bidirectional and central to understanding the target organ toxicity of mercury. An addition critical feature of mercury toxicity and of the interaction with selenium is the chemical state of mercury (e.g., Hg0, Hg+, and Hg+2). The mechanism of toxicity of mercury is based on its ability to bind to and in certain cases inhibit moieties containing sulfur and selenium [3–5,10]. Mercury has a lower affinity for thiol groups and higher affinity for selenium containing groups, allowing for binding in a multifaceted way. The relative ease with which mercury can move from one thiol group to another allows for movement from one binding group to another, transport across membranes, and potentially temporarily impairment of multiple proteins [10]. The binding of mercury to selenium on selenoproteins and selenoenzymes is of higher affinity by several orders of magnitude and more stable when compared to its binding with thiol groups, making these the final or primary target of mercury [5,11,12].
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