Prolonged central sensory conduction time in patients with chronic arsenic exposure

Mochizuki, Hitoshi; Yagi, Kazuhiro; Tsuruta, Kazuhito; Taniguchi, Akitoshi; Ishii, Nobuyuki; Shiomi, Kazutaka; Nakazato, Masamitsu

doi:10.1016/j.jns.2015.12.020

Cited by 19 publications

(17 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As mentioned above, several studies have shown that arsenic exposure induces peripheral neuropathy or neuritis [7, 9, 22–24]. A few studies have separately analyzed the function of small and large fibers, and suggested that these particular effects of arsenic are specific to small fibers [6, 9, 10]. Large-fiber function can be evaluated not only by neurological examination of vibration sensation but also by nerve conduction studies.…”

Section: Discussionmentioning

confidence: 99%

“…At least 140 million people in more than 50 countries are exposed to arsenic-contaminated drinking water [3]. Chronic arsenic toxicity induces not only cardiovascular disease, skin lesions, diabetes, and cancers of the kidney, skin, and bladder [1, 4, 5] but also central and peripheral nervous system impairments [6–9].…”

Section: Introductionmentioning

confidence: 99%

“…In regard to the peripheral nervous system, a considerable number of patients who experience chronic arsenic exposure report subjective complaints of numbness or tingling [7, 10], but nerve conduction studies reveal no abnormal findings [11]. As for the central nervous system, the central sensory conduction time of patients with chronic arsenic exposure is longer than that in age-matched normal controls [6]. Neurobehavioral functions are impaired in patients aged 12–16 years who have experienced chronic arsenic exposure [8].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Peripheral neuropathy induced by drinking water contaminated with low-dose arsenic in Myanmar

Mochizuki

Phyu

Aung

et al. 2019

Environ Health Prev Med

Self Cite

View full text Add to dashboard Cite

Background More than 140 million people drink arsenic-contaminated groundwater. It is unknown how much arsenic exposure is necessary to cause neurological impairment. Here, we evaluate the relationship between neurological impairments and the arsenic concentration in drinking water (ACDW). Participants and methods A cross-sectional study design was employed. We performed medical examinations of 1867 residents in seven villages in the Thabaung township in Myanmar. Medical examinations consisted of interviews regarding subjective neurological symptoms and objective neurological examinations of sensory disturbances. For subjective neurological symptoms, we ascertained the presence or absence of defects in smell, vision, taste, and hearing; the feeling of weakness; and chronic numbness or pain. For objective sensory disturbances, we examined defects in pain sensation, vibration sensation, and two-point discrimination. We analyzed the relationship between the subjective symptoms, objective sensory disturbances, and ACDW. Results Residents with ACDW ≥ 10 parts per billion (ppb) had experienced a “feeling of weakness” and “chronic numbness or pain” significantly more often than those with ACDW < 10 ppb. Residents with ACDW ≥ 50 ppb had three types of sensory disturbances significantly more often than those with ACDW < 50 ppb. In children, there was no significant association between symptoms or signs and ACDW. Conclusion Subjective symptoms, probably due to peripheral neuropathy, occurred at very low ACDW (around 10 ppb). Objective peripheral nerve disturbances of both small and large fibers occurred at low ACDW (> 50 ppb). These data suggest a threshold for the occurrence of peripheral neuropathy due to arsenic exposure, and indicate that the arsenic concentration in drinking water should be less than 10 ppb to ensure human health.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Peripheral neuropathy induced by drinking water contaminated with low-dose arsenic in Myanmar

Mochizuki

Phyu

Aung

et al. 2019

Environ Health Prev Med

Self Cite

View full text Add to dashboard Cite

show abstract

“…This discrepancy could not be explained solely by the age-related impairment of large peripheral nerves. Indeed, two studies that evaluated sensory disturbance in residents of Toroku demonstrated central nervous system dysfunction (Mochizuki et al 2016 ) and small fiber neuropathy (Kawasaki et al 2002 ). Although the detailed mechanisms are unclear, these conditions may have contributed to the gradual sensory impairment.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, huge amounts of arsenic trioxide-containing gases were leaked from the roasters and intermittently covered the entire Toroku valley, causing both refinery workers and residents to be exposed to arsenic orally (via contaminated food and water), dermally, or tracheally (via contaminated air) (Miyazaki prefecture 1972 ; Tsuda et al 1990 ). The polluted environment caused chronic arsenic intoxication in many workers and residents, leading to many deaths before 1962 (Miyazaki prefecture 1972 ; Mochizuki et al 2016 ). In 1972, 10 years after the mine closed, arsenic concentrations were finally measured by Miyazaki prefecture.…”

mentioning

confidence: 99%

Clinical Symptoms, Neurological Signs, and Electrophysiological Findings in Surviving Residents with Probable Arsenic Exposure in Toroku, Japan

Ishii

Mochizuki

Ebihara

et al. 2018

Arch Environ Contam Toxicol

Self Cite

View full text Add to dashboard Cite

Chronic arsenic intoxication is known to cause multisystem impairment and is still a major threat to public health in many countries. In Toroku, a small village in Japan, arsenic mines operated from 1920 to 1962, and residents suffered serious sequelae of arsenic intoxication. We have performed annual medical examinations of these residents since 1974, allowing us to characterize participants’ long-term health following their last exposure to arsenic. The participants could not be described as having “chronic arsenic intoxication,” because their blood arsenic levels were not measured. In this study, we defined them as having “probable arsenic intoxication.” Symptoms frequently involved the sensory nervous system, skin, and upper respiratory system (89.1–97.8%). In an analysis of neurological findings, sensory neuropathy was common, and more than half of the participants complained of hearing impairment. Longitudinal assessment with neurological examinations and nerve conduction studies revealed that sensory dysfunction gradually worsened, even after exposure cessation. However, we could not conclude that arsenic caused the long-term decline of sensory function due to a lack of comparisons with age-matched healthy controls. This is the first study to characterize the longitudinal sequelae after probable arsenic exposure. Our study will be helpful to assess the prognosis of patients worldwide who still suffer from chronic arsenic intoxication.

show abstract

Nerve growth factor prevents arsenic‐induced toxicity in PC12 cells through the AKT/GSK‐3β/NFAT pathway

Tan

Kang

Zhang

et al. 2018

Journal Cellular Physiology

View full text Add to dashboard Cite

The potential risk of arsenic-related neurodegeneration has been a growing concern. Arsenic exposure has been reported to disrupt neurite growth and neuron body integrity in vitro; however, its underlying mechanism remains unclear. Previously, we showed that arsenic sulfide (AS) exerted cytotoxicity in gastric and colon cancer cells through regulating nuclear factor of the activated T cells (NFAT) pathway. The NFAT pathway regulates axon path finding and neural development. Using neural crest cell line PC12 cells as a model, here we show that AS caused mitochondrial membrane potential collapse, reactive oxygen species production, and cytochrome c release, leading to mitochondria-mediated apoptosis via the AKT/GSK-3β/NFAT pathway. Increased glycogen synthase kinase-3 beta (GSK-3β) activation leads to the inactivation of NFAT and its antiapoptotic effects. Through inhibiting GSK-3β activity, both nerve growth factor (NGF) and Tideglusib, a GSK-3β inhibitor partially rescued the PC12 cells from the AS-induced cytotoxicity and restored the expression of NFATc3. In addition, overexpression of NFATc3 stimulated neurite outgrowth and potentiated the effect of NGF on promoting the neurite outgrowth. Collectively, our results show that NFATc3 serves as the downstream target of NGF and plays a key role in preventing AS-induced neurotoxicity through regulating the AKT/GSK-3β/NFAT pathway in PC12 cells.

show abstract

Prolonged central sensory conduction time in patients with chronic arsenic exposure

Abstract: This is the first study to identify an impairment of the central somatosensory pathway in patients with chronic arsenic exposure. Sensory disturbance in these patients is related not only to peripheral neuropathy but also to impairment of the central nervous system.

Cited by 19 publications

References 19 publications

Peripheral neuropathy induced by drinking water contaminated with low-dose arsenic in Myanmar

Peripheral neuropathy induced by drinking water contaminated with low-dose arsenic in Myanmar

Clinical Symptoms, Neurological Signs, and Electrophysiological Findings in Surviving Residents with Probable Arsenic Exposure in Toroku, Japan

Nerve growth factor prevents arsenic‐induced toxicity in PC12 cells through the AKT/GSK‐3β/NFAT pathway

Contact Info

Product

Resources

About