cutaneous and auditory function in rats following methyl mercury poisoning

Wu, Ming-Fung; Ison, James R.; Wecker, John R.; Lapham, Lowell W.

doi:10.1016/0041-008x(85)90136-x

Cited by 42 publications

(18 citation statements)

References 27 publications

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“…Also, the differential performance in PA could be related with the potential effects of MeHg on (electric) shock sensitivity, which we did not examine. At least one high-dose study with adult rats showed reduced electric sensitivity due to mercury exposure (Wu et al 1985). These possibilities need to be addressed in future studies.…”

Section: Discussionmentioning

confidence: 99%

Emergence of Delayed Methylmercury Toxicity after Perinatal Exposure in Metallothionein-Null and Wild-Type C57BL Mice

Yoshida

Shimizu

Suzuki

et al. 2008

Environ Health Perspect

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BackgroundAlthough a long latency period of toxicity after exposure to methylmercury (MeHg) is known to exist in humans, few animal studies have addressed this issue. Substantiation of delayed MeHg toxicity in animals would affect the risk evaluation of MeHg.ObjectivesOur goal in this study was to demonstrate the existence of a latency period in a rodent model in which the toxicity of perinatal MeHg exposure becomes apparent only later in life. Our study included metallothionein (MT) knockout mice because studies have suggested the potential susceptibility of this strain to the neurodevelopmental toxicity of MeHg.MethodsPregnant MT-null and wild-type C57Bl/6J mice were exposed to MeHg through their diet containing 5 μg Hg/g during gestation and early lactation. We examined behavioral functions of the offspring using frequently used paradigms, including open field behavior (OPF), passive avoidance (PA), and the Morris water maze (MM), at ages of 12–13 and 52–53 weeks.ResultsAt 12 weeks of age, behavioral effects of MeHg were not detected, except for OPF performance in MeHg-exposed MT-null females. At 52 weeks of age, the MeHg-exposed groups showed poorer performance both in PA and MM, and their OPF activity differed from controls. These effects of MeHg appeared exaggerated in the MT-null strain. The brain Hg concentration had leveled off by 13 weeks of age.ConclusionsThe results suggest the existence of a long latency period after perinatal exposure to low-level MeHg, in which the behavioral effects emerged long after the leveling-off of brain Hg levels. Hence, the initial toxicologic event responsible for the late effects should have occurred before this leveling-off of brain Hg.

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Section: Discussionmentioning

confidence: 99%

Emergence of Delayed Methylmercury Toxicity after Perinatal Exposure in Metallothionein-Null and Wild-Type C57BL Mice

Yoshida

Shimizu

Suzuki

et al. 2008

Environ Health Perspect

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“…The effects of mercury poisoning effects in the central nervous system include depression, paranoia, extreme irritability, hallucinations, an inability to concentrate, memory loss, tremors of the hands, head, lips, tongue, jaw and eyelids, weight loss, perpetually low body temperature, drowsiness, headaches, insomnia, and fatigue. Along with nervous system effects, mercury has also shown to have various effects on other special sensory systems including blindness, retinopathy, optic neuropathy, hearing loss, a reduced sense of smell, and abnormal touch sensation [54]. Autism is a syndrome characterized by impairments in social relatedness, language and communication, a need for routine and sameness, abnormal movements, and sensory dysfunction [55].…”

Section: Effects On the Nervous Systemmentioning

confidence: 99%

Environmental Mercury and Its Toxic Effects

Rice

Walker

et al. 2014

J Prev Med Public Health

890

426

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Mercury exists naturally and as a man-made contaminant. The release of processed mercury can lead to a progressive increase in the amount of atmospheric mercury, which enters the atmospheric-soil-water distribution cycles where it can remain in circulation for years. Mercury poisoning is the result of exposure to mercury or mercury compounds resulting in various toxic effects depend on its chemical form and route of exposure. The major route of human exposure to methylmercury (MeHg) is largely through eating contaminated fish, seafood, and wildlife which have been exposed to mercury through ingestion of contaminated lower organisms. MeHg toxicity is associated with nervous system damage in adults and impaired neurological development in infants and children. Ingested mercury may undergo bioaccumulation leading to progressive increases in body burdens. This review addresses the systemic pathophysiology of individual organ systems associated with mercury poisoning. Mercury has profound cellular, cardiovascular, hematological, pulmonary, renal, immunological, neurological, endocrine, reproductive, and embryonic toxicological effects.

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“…Auditory brainstem response (ABR) test, a method to provide a clear and reliable indicator of hearing function in the central auditory system, is a useful indicator of neurotoxicity in body burdens of toxic metals [15, 16]. It has been demonstrated the significant correlation between the abnormal ABR test (the hearing loss and the latency of wave III and V delayed) and Hg accumulation during prenatal, postnatal, development, adult stage exposed to mercury or existed in patients with mercury-contaminated area [2, 17–20].…”

Section: Introductionmentioning

confidence: 99%

“…It has been demonstrated the significant correlation between the abnormal ABR test (the hearing loss and the latency of wave III and V delayed) and Hg accumulation during prenatal, postnatal, development, adult stage exposed to mercury or existed in patients with mercury-contaminated area [2, 17–20]. In experimental animals, the irreversible loss of hearing after exposure to chemicals (such as MeHg or cisplatin) has been reported to be associated with toxicity to the central auditory system, including auditory loss or damage to the cochlea [16, 21, 22]. However, possible ototoxic effects of low dose of cinnabar exposure remain unclear, especially during the perinatal or developmental periods.…”

Section: Introductionmentioning

confidence: 99%

Exposure to Low Dose of Cinnabar (a Naturally Occurring Mercuric Sulfide (HgS)) Caused Neurotoxicological Effects in Offspring Mice

Huang

Hsu

Liu

et al. 2012

Journal of Biomedicine and Biotechnology

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Cinnabar, a naturally occurring mercuric sulfide (HgS), has long been used in Chinese mineral medicine for more than 2000 years. Although mercury is well-known for its toxicity, whether cinnabar induces neurotoxicity, especially in infants and children, is unknown. The purpose of this study was to explore the neurotoxic effects of low-dose of cinnabar (10 mg/kg/day) on developing mice. The results revealed neurobehavioral defects in F1-C-Cin group, which were associated with Hg accumulation, increased NOx levels in whole blood, and Na+/K+-ATPase activities in brain tissues. F1- and F2-Cin-V groups were found to increase brain Hg contents and prominent neurobehavioral defects compared with F1-C-V group, suggesting that the fetal brain was more susceptible to irreversible effects for cinnabar-induced damage. Moreover, F1- and F2-Cin-Cin groups had severely neurobehavioral dysfunctions, closely correlated with the further alteration of NOx levels and Na+/K+-ATPase activities than F1- and F2-C-Cin groups. Effects in F2-Cin-Cin group were more significant than those in F1-Cin-Cin group. In conclusion, this study demonstrates that exposure to low-dose of cinnabar during the perinatal and developmental stages results in irreversible and severe injuries of the neurotoxicity in offspring, and NOx and Na+/K+-ATPase activities may exist potential and useful biomarkers for neurotoxicity-induced by low-doses of mercuric compounds.

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cutaneous and auditory function in rats following methyl mercury poisoning

Cited by 42 publications

References 27 publications

Emergence of Delayed Methylmercury Toxicity after Perinatal Exposure in Metallothionein-Null and Wild-Type C57BL Mice

Emergence of Delayed Methylmercury Toxicity after Perinatal Exposure in Metallothionein-Null and Wild-Type C57BL Mice

Environmental Mercury and Its Toxic Effects

Exposure to Low Dose of Cinnabar (a Naturally Occurring Mercuric Sulfide (HgS)) Caused Neurotoxicological Effects in Offspring Mice

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