Mercury (Hg2+) suppression of potassium currents of outer hair cells

Guihua, Liang; Järlebark, Leif; Ulfendahl, Mats; Moore, Ernest J.

doi:10.1016/s0892-0362(03)00008-4

Cited by 37 publications

(17 citation statements)

References 38 publications

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“…Since mercury has been proposed to be ototoxic, we hypothesized that these high mercury levels would correlate with hearing loss [Anniko and Sarkady, 1978;Liang et al, 2003;Rothwell and Boyd, 2008;Wassick and Yonovitz, 1985]. However, we did not find any significant relationships between mercury levels and hearing parameters, but we did find that many metal levels were elevated in addition to mercury.…”

Section: Discussioncontrasting

confidence: 64%

Hearing Loss and Heavy Metal Toxicity in a Nicaraguan Mining Community: Audiological Results and Case Reports

et al. 2012

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We measured fingernail metal levels, Békésy-type pure-tone thresholds and distortion product otoacoustic emission (DPOAE) levels in 59 subjects residing in the gold mining community of Bonanza, Nicaragua. Auditory testing revealed widespread hearing loss in the cohort. Nail metal concentrations (mercury, lead, aluminum, manganese and arsenic) far exceeded reference levels. No relationship was found between metal levels and auditory test results for the group as a whole. Statistically significant relationships were found between DPOAE response amplitudes and metal concentrations in a subgroup with less than 40 h per week of significant noise exposure; however, conclusions regarding these relationships should be tempered by the large number of analyses performed. Several young individuals with high metal levels reported neurological symptoms and had poor hearing. The data suggest that metal levels in artisanal mining communities present a significant public health problem and may affect hearing.

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Section: Discussioncontrasting

confidence: 64%

Hearing Loss and Heavy Metal Toxicity in a Nicaraguan Mining Community: Audiological Results and Case Reports

et al. 2012

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“…These data support the hypothesis that AQPs in the vesicle membrane facilitate the rapid influx of water by greatly increasing the permeability of the vesicle membrane to water. However, it should be noted that Hg 2+ can have inhibitory effects on a variety of other transporters including K + channels (Gallagher et al, 1995;Leonhardt et al, 1996;Liang et al, 2003), Na + channels (Kurata et al, 1998;Leonhardt et al, 1996), Ca 2+ channels (Leonhardt et al, 1996;Pekel et al, 1993) and Na-K-2Cl cotransporters (Kinne-Saffran and Kinne, 2001). However, given that Hg 2+ caused a reduction in swelling rate, and not the inhibition of rupture, as was seen with other chemical inhibitors (DIDS, tannic acid and PGG), ion flux was likely not affected.…”

Section: Sus Scrofa Aqp6 [Acc66198]mentioning

confidence: 99%

Defensive slime formation in Pacific hagfish requires Ca2+ and aquaporin mediated swelling of released mucin vesicles

Herr

Clifford

Goss

et al. 2014

Journal of Experimental Biology

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Hagfishes defend themselves from fish predators via the rapid deployment of a fibrous slime that adheres to and clogs gills. The slime transforms from a thick glandular exudate to a fully hydrated product in a fraction of a second through a process that involves the swelling and rupture of numerous mucin vesicles. Here we demonstrate that the vesicle membrane plays an important role in regulating the swelling of mucin granules, and provide evidence that the membrane contains proteins that facilitate the movement of ions and water molecules. By exposing isolated mucin vesicles to varying combinations of inorganic ions, organic compounds and membrane channel inhibitors, we found that the majority of hagfish mucin vesicles require Ca 2+ to rupture. We also show that Ca 2+-dependent rupture can be pharmacologically inhibited, which suggests a role for Ca 2+ -activated membrane transporters. We demonstrate that the aquaporin inhibitor mercuric chloride reduces the rate of vesicle swelling by an order of magnitude, which suggests that aquaporins facilitate the influx of water during vesicle deployment. Molecular evidence of two aquaporin homologues expressed in the slime glands further supports this idea. We propose a model of hagfish slime mucin vesicle rupture that involves Ca 2+ -activated transporters and aquaporins, and suggest that the presence of these proteins is an adaptation for increasing the speed of vesicle rupture and, consequently, the speed of the sliming response of hagfishes.

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“…The existence of inorganic mercury in the motor axon may directly lead to a dysfunction of the ion channels in the nerves. In animal and in vitro studies, both organic and inorganic mercury can suppress the function of ion channels [29,30,31,32,33]. VGCCs are particularly vulnerable because Ca 2+ has a similar chemical structure to Hg 2+ .…”

Section: Literature Review and Discussionmentioning

confidence: 99%

Subacute Motor Neuron Hyperexcitability with Mercury Poisoning: A Case Series and Literature Review

et al. 2014

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Motor neuron hyperexcitability (MNH) indicates a disorder characterized by an ectopic motor nerve discharge on electromyogram (EMG). Here, we present a series of three cases of subacute MNH with mercury poisoning. The first case showed hyperhidrosis, insomnia, generalied myokymia, cramps, tremor, weight loss, and myokymic and neuromyotonic discharges, followed by encephalopathy with confusion, hallucinations, and memory decrease. The second case was similar to the former but without encephalopathic features. The third case showed widespread fasciculation, fatigue, insomnia, weight loss, and autonomic dysfunction, including constipation, micturition difficulty, and impotence, with multiple fibrillation, unstable fasciculation, widened motor neuron potential, and an incremental response at high-rate stimulation in repetitive nerve stimulation. Based on the symptoms, the three cases were diagnosed as Morvan's syndrome, Isaacs' syndrome, and Lambert-Eaton myasthenic syndrome with ALS-like syndrome, respectively. Mercury poisoning in the three cases was confirmed by analysis of blood and urine samples. All cases recovered several months after chelation therapy and were in good condition at follow-up. Very few cases of MNH linked with mercury exposure have been reported in the literature. The mechanism of mercury-induced MNH may be associated with ion channel dysfunction.

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Mercury (Hg2+) suppression of potassium currents of outer hair cells

Cited by 37 publications

References 38 publications

Hearing Loss and Heavy Metal Toxicity in a Nicaraguan Mining Community: Audiological Results and Case Reports

Hearing Loss and Heavy Metal Toxicity in a Nicaraguan Mining Community: Audiological Results and Case Reports

Defensive slime formation in Pacific hagfish requires Ca2+ and aquaporin mediated swelling of released mucin vesicles

Subacute Motor Neuron Hyperexcitability with Mercury Poisoning: A Case Series and Literature Review

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