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Free Radicals and Antioxidants
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Manganese (Mn) is an essential micronutrient and a trace metal that intervenes in the activity of superoxide dismutase within the mitochondria (111, 214–215). Superoxide dismutase (SOD) is a metalloenzyme and antioxidant enzyme. SOD contains metal such as manganese, copper, zinc, or iron, used as cofactor for the enzyme’s functioning. SOD protects cells from reactive oxygen species (ROS) by decomposing superoxide radical O2.- into molecular oxygen (O2) and hydrogen peroxide (H2O2) by cyclic oxidation and reduction reactions with the active site metal (214–215). In humans, there are three forms of SODs: SOD-1, SOD-2, and SOD-3. SOD1 and SOD3 contain copper and zinc and are located in the cytoplam and the endoplasm, respectively. As for SOD-2, it contains manganese as cofactor and is located in the mitochondria. SOD-2 or Mn-SOD is of great interest to the medical field because of its protection against the deleterious effects of excessive superoxide in disease states (214). Decreased levels of SOD-2 may contribute to the development of certain diseases such as neurodegenerative diseases (Parkinson’s disease and amyotrophic lateral sclerosis), diabetes, and cancer (214–215). Mn deficiency in the body leads to the inactivation of SOD-2 antioxidant enzyme. However, chronic exposure to Mn causes manganism, a manganese poisoning that is a classic ‘pro-oxidant’ disease.
Inhalation Toxicity of Metal Particles and Vapors
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Chronic manganese toxicity (“manganism”) is well known in miners, mill-workers, and others exposed to dust and fumes. The usual signs and symptoms involve the central nervous system. This disease is reversible if recognized very early and if exposure to dust of Mn oxides is eliminated. However, after the onset of the disease, the neurological symptoms remain, even after the exposure to Mn is removed and the tissue Mn levels revert to normal. A peculiar slapping gait, cramps or tremors of the body and extremities, slurred speech, hallucinations, insomnia, mental confusion are some of the symptoms. At this stage, the symptoms resemble those of Parkinson’s disease (Cotzias, 1958). In spite of the severity of the symptoms, manganism is not fatal, although it causes premanent disability.
The Effects of Pollution, Toxins, and Diet on Behavior
Published in Gail S. Anderson, Biological Influences on Criminal Behavior, 2019
Manganese is an essential nutrient involved in brain development and in the metabolism of lipids, proteins, and amino acid, but in excess it can be toxic to the neurological system.58 Severe exposure can lead to symptoms similar to those of Parkinson’s disease, known as parkinsonian symptoms, affecting motor and cognitive skills. In severe cases, it can lead to manganism.59 Even at less severe levels of exposure, it has been shown to be neurotoxic. It can accumulate in the brain and affect the dopaminergic and serotonergic systems, reducing the levels of dopamine, serotonin, and other neurotransmitters,60 which, as we know from Chapter 9, can affect impulsivity and antisocial behavior. Animal studies have shown that young animals accumulate higher concentrations of manganese in the brain than adults and that manganese accumulates particularly in the prefrontal cortex, cerebellum, hippocampus, and basal ganglia, all of which are important in working memory and hence learning and cognitive skills (reviewed in Khan, Wasserman, et al.61). It is also accumulated in the mitochondria and so can impact MAO synthesis.62
Biomarkers for occupational manganese exposure
Published in Critical Reviews in Toxicology, 2022
Nataliya A. Karyakina, Natalia Shilnikova, Nawal Farhat, Siva Ramoju, Brandon Cline, Franco Momoli, Donald Mattison, N. Jensen, R. Terrell, Daniel Krewski
Long-term occupational inhalation exposure to high levels of insoluble Mn oxide dust or fume particulates may lead to an excessive Mn accumulation in the basal ganglia of the brain and the development of a clinical condition called manganism (ATSDR 2012). Classical fully developed manganism is characterized by tremor, dysdiadochokinesia, ataxic gait, dystonia, and cogwheel phenomenon (postural tremor) (ATSDR 2012). “Cock walk” is generally considered as a clinical sign that is specific to Mn neurotoxicity (Calne et al. 1994; Jankovic 2005). It has been suggested that neurological symptoms may improve in some cases if a patient is removed from Mn exposure at an early stage (e.g. cognitive, (Ky et al. 1992)); however, clinical progression of motor functions impairment tends to persist and may even worsen after cessation of exposure (Huang et al. 1998). Clinical signs and symptoms of manganism are similar to Parkinson’s Disease (PD) with some clinical, pharmacological, and imaging differences (see Calne et al. (1994) for a detailed discussion of the differences).
Manganese concentration in patients with encephalopathy following ephedrone use: a narrative review and analysis of case reports
Published in Clinical Toxicology, 2022
Michal Ordak, Natalia Sloniewicz, Tadeusz Nasierowski, Elzbieta Muszynska, Magdalena Bujalska-Zadrozny
The maximum daily non-toxic dose of manganese is 9–11 mg per day for adults [3]. Occupational exposure to manganese mainly occurs during the extraction and processing of manganese ores, alloy production, at steel mills, during welding and dry cell production. Therefore, manganese ore miners and smelters involved in casting and refining are particularly vulnerable [4–6]. Manganism is a neurological disorder characterized by mood swings and an extrapyramidal syndrome similar to Parkinson's disease. Long-term exposure to lower doses of manganese may lead to an increased frequency of Parkinsonian symptoms [7]. Less common neurological symptoms of manganism include palilalia (involuntary word repetition), hypomimia (mask-like loss of facial expression), as well as bradyphrenia (slowed cognitive processing) [8,9]. Exposure to high levels of manganese in the workplace can also lead to long-term movement, cognitive and behavioural disorders. Most patients suffer from impaired speech, gait and posture and have difficulty walking backwards [10]. Exposure to manganese in the workplace is phenotypically similar to exposure to high levels of manganese with ephedrone [11].
The neuroprotective properties of carnosine in a mouse model of manganism is mediated via mitochondria regulating and antioxidative mechanisms
Published in Nutritional Neuroscience, 2020
Mohammad Mehdi Ommati, Reza Heidari, Vahid Ghanbarinejad, Ahmadreza Aminian, Narges Abdoli, Hossein Niknahad
Manganese (Mn) is an essential trace element. Physiologically, Mn is a constituent of many important metalloenzymes in the human body and incorporates in several metabolic processes.1 Despite its essentiality, excess Mn exposure could lead to significant neurotoxicity.2–8 Mn exposure occurs in several ways including air born Mn-containing particulates, Mn-based pesticides, or drinking water.9,10 Elevated body Mn level is also associated with several liver diseases especially cirrhosis and chronic bile duct injury.11–15 Mn-induced neurotoxicity syndrome is known as ‘manganism’.16 Manganism is associated with a wide range of locomotor dysfunction and cognitive deficits.1–5,7,13 It has been found that alterations in dopaminergic neurons compromise motor function upon Mn exposure.1–5,7,13