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    Four cases of abnormal neuropsychological findings in children with high blood methylmercury concentrations. Hong Young-Seoub,Kim Dae-Seon,Yu Seung-Do,Kim Seong-Hwan,Kim Jong-Kuk,Kim Yu-Mi,Yu Jae-Ho,Jung Ji-Hyun,Kim Byoung-Gwon Annals of occupational and environmental medicine BACKGROUND:Methylmercury (MeHg) easily crosses the blood-brain barrier and accumulates in the brain. Accumulated MeHg will cause neurological symptoms. We report four pediatric cases of neuropsychological findings with high blood MeHg concentrations. CASE PRESENTATION:Four children were admitted for follow-up study because their total mercury (THg) concentration in the blood was found to be high during a national survey. Case 1 was a 9-year-old female with a 16.6 μg/ℓ blood THg concentration in the survey. During admission, the blood THg, hair THg, and blood MeHg concentration(mercury indices) were 21.4 μg/ℓ, 7.2 μg/g, and 20.1 μg/ℓ, respectively. In our neuropsychological examination, cognitive impairment and attention deficit were observed. Her diet included fish intake 2-3 times per week, and she had been diagnosed with epilepsy at 3 years of age. Case 2 was a 12-year-old male with blood THg of 15.4 μg/ℓ in the survey and the mercury indices were 12.7 μg/ℓ, 5.7 μg/g, and 11.8 μg/ℓ, respectively, on admission. He was also observed to have attention-deficit/hyperactivity disorder. Case 3 was a 10-year-old male child with blood THg of 17.4 μg/ℓ in the survey, and the mercury indices on admission were 21.6 μg/ℓ, 7.5 μg/g and 21.5 μg/ℓ, respectively. In his case, mild attention deficit was observed. Case 4 was a 9-year-old male with blood THg of 20.6 μg/ℓ in the survey and the mercury indices were 18.9 μg/ℓ, 8.3 μg/g, and 14.4 μg/ℓ, respectively, on admission. Mild attention difficulty was observed. CONCLUSION:We suggest that fish consumption may be the main source of MeHg exposure, and that MeHg may have been the cause of the neuropsychological deficits in these cases. 10.1186/2052-4374-25-18
    A review for the pharmacological effect of lycopene in central nervous system disorders. Chen Dongjian,Huang Chao,Chen Zhuo Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie Lycopene is an aliphatic hydrocarbon carotenoid extracted from plants like tomatoes, papayas, and watermelons. Previous studies have shown that lycopene can exert prophylactic and/or therapeutic effects in different disorders, such as heart failure and neoplasm via anti-oxidative, anti-inflammatory, and anti-proliferative activities. In the central nervous system (CNS), lycopene also has prophylactic and/or therapeutic effects in different type of disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), cerebral ischemia, epilepsy, and depression. Lycopene also improves cognition and memory ability of rodents in different pathological conditions, such as diabetes, colchicine exposure, high-fat diet (HFD), and aging. Further, lycopene can prevent neuro-toxicities induced by monosodium glutamate (MSG), trimethyltin (TMT), methylmercury (MeHg), tert-butyl hydroperoxide (t-BHP), and cadmium (Cd). In some special conditions such as ethanol addiction and haloperidol-induced orofacial dyskinesia, lycopene administration displays special therapeutic effects. Mechanisms including inhibition of oxidative stress and neuroinflammation, inhibition of neuronal apoptosis, and restoration of mitochondrial function have been shown to mediate the neuroprotective effects of lycopene. Other mechanisms, such as inhibition of nuclear factor-κB (NF-κB) and c-Jun N-terminal kinase (JNK), activation of the nuclear factor erythroid 2-related factor (Nrf2) and brain-derived neurotrophic factor (BDNF) signaling, and restoration of intracellular Ca homeostasis, may be also involved in the neuroprotective effect of lycopene. In hope of get a clear impression about the role of lycopene in the CNS, we summarize and discuss the pharmacological effects of lycopene as well as its possible mechanisms in CNS disorder prevention and/or therapy. 10.1016/j.biopha.2018.12.151
    Effect of chronic low-dose developmental methylmercury intoxication on epileptogenicity in rats. Szász A,Barna B,Galbács Z,Kirsch-Volders M,Szente M Central European journal of public health