Lead exposure results in hearing loss and disruption of the cochlear blood–labyrinth barrier and the protective role of iron supplement

Liu, Xinqin; Zheng, Gang; Wu, Yong-Xiang; Shen, Xuefeng; Jing, Jinfei; Yu, Tao; Song, Han; Chen, Jingyuan; Luo, Wenjing

doi:10.1016/j.neuro.2013.10.002

Cited by 34 publications

(28 citation statements)

References 54 publications

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“…Iron supplement contributes to maintaining the integrity of the blood-labyrinth barrier and the homeostasis in the cochlea [32]. The main iron-related gene variants, such as FPN1 (ferroportin), TF (transferrin), HFE (human hemochromatosis gene), and HEPC / HAMP (hepcidin), may be significantly associated with increased risk of developing sudden hearing loss [33].…”

Section: Discussionmentioning

confidence: 99%

Low Iron Diet Increases Susceptibility to Noise-Induced Hearing Loss in Young Rats

Hao

Yang

et al. 2016

Nutrients

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We evaluated the role of iron deficiency (ID) without anemia on hearing function and cochlear pathophysiology of young rats before and after noise exposure. We used rats at developmental stages as an animal model to induce ID without anemia by dietary iron restriction. We have established this dietary restriction model in the rat that should enable us to study the effects of iron deficiency in the absence of severe anemia on hearing and ribbon synapses. Hearing function was measured on Postnatal Day (PND) 21 after induction of ID using auditory brainstem response (ABR). Then, the young rats were exposed to loud noise on PND 21. After noise exposure, hearing function was again measured. We observed the morphology of ribbon synapses, hair cells and spiral ganglion cells (SGCs), and assessed the expression of myosin VIIa, vesicular glutamate transporter 3 and prestin in the cochlea. ID without anemia did not elevate ABR threshold shifts, but reduced ABR wave I peak amplitude of young rats. At 70, 80, and 90 dB SPL, amplitudes of wave I (3.11 ± 0.96 µV, 3.52 ± 1.31 µV, and 4.37 ± 1.08 µV, respectively) in pups from the ID group were decreased compared to the control (5.92 ± 1.67 µV, 6.53 ± 1.70 µV, and 6.90 ± 1.76 µV, respectively) (p < 0.05). Moreover, ID without anemia did not impair the morphology hair cells and SGCs, but decreased the number of ribbon synapses. Before noise exposure, the mean number of ribbon synapses per inner hair cell (IHC) was significantly lower in the ID group (8.44 ± 1.21) compared to that seen in the control (13.08 ± 1.36) (p < 0.05). In addition, the numbers of ribbon synapses per IHC of young rats in the control (ID group) were 6.61 ± 1.59, 3.07 ± 0.83, 5.85 ± 1.63 and 12.25 ± 1.97 (3.75 ± 1.45, 2.03 ± 1.08, 3.81 ± 1.70 and 4.01 ± 1.65) at 1, 4, 7 and 14 days after noise exposure, respectively. Moreover, ABR thresholds at 4 and 8 kHz in young rats from the ID group were significantly elevated at 7 and 14 days after noise exposure compared to control (p < 0.05). The average number of young rat SGCs from the ID group were significantly decreased in the basal turn of the cochlea compared to the control (p < 0.05). Therefore, ID without anemia delayed the recovery from noise-induced hearing loss and ribbon synapses damage, increased SGCs loss, and upregulated prestin after noise exposure. Thus, the cochleae in rat pups with ID without anemia were potentially susceptible to loud noise exposure, and this deficit may be attributed to the reduction of ribbon synapses and SGCs.

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Section: Discussionmentioning

confidence: 99%

Low Iron Diet Increases Susceptibility to Noise-Induced Hearing Loss in Young Rats

Hao

Yang

et al. 2016

Nutrients

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“…Exposure to low levels of lead during development decreased the expression of voltage-dependent anion channel proteins and disrupted the monoaminergic system in the auditory brainstem (Fortune and Lurie, 2009; Prins et al, 2010a,b). Furthermore, lead exposure induced degeneration of sensory receptor cells in the cochlea, affected auditory nerve conduction velocity, disrupted cochlear blood-labyrinth barrier, and caused vestibular dysfunction (Jones et al, 2008; Klimpel et al, 2017; Lasky et al, 1995; Liu et al, 2013; Yamamura et al, 1989). Despite these overwhelming evidences indicating the ototoxic effects of lead, the underlying mechanism is yet to be fully understood.…”

Section: Introductionmentioning

confidence: 99%

Chronic lead exposure induces cochlear oxidative stress and potentiates noise-induced hearing loss

et al. 2018

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Acquired hearing loss is caused by complex interactions of multiple environmental risk factors, such as elevated levels of lead and noise, which are prevalent in urban communities. This study delineates the mechanism underlying lead-induced auditory dysfunction and its potential interaction with noise exposure. Young-adult C57BL/6 mice were exposed to: 1) control conditions; 2) 2 mM lead acetate in drinking water for 28 days; 3) 90 dB broadband noise 2 h/day for two weeks; and 4) both lead and noise. Blood lead levels were measured by inductively coupled plasma mass spectrometry analysis (ICP-MS) lead-induced cochlear oxidative stress signaling was assessed using targeted gene arrays, and the hearing thresholds were assessed by recording auditory brainstem responses. Chronic lead exposure downregulated cochlear Sod1, Gpx1, and Gstk1, which encode critical antioxidant enzymes, and upregulated ApoE, Hspa1a, Ercc2, Prnp, Ccl5, and Sqstm1, which are indicative of cellular apoptosis. Isolated exposure to lead or noise induced 8–12 dB and 11–25 dB shifts in hearing thresholds, respectively. Combined exposure induced 18–30 dB shifts, which was significantly higher than that observed with isolated exposures. This study suggests that chronic exposure to lead induces cochlear oxidative stress and potentiates noise-induced hearing impairment, possibly through parallel pathways.

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“…NEURODEVELOPMENTAL DISORDERS Studies in animal models have been generally consistent with adverse auditory effects of lead exposure. Post-weaning exposures of mice yielding blood lead values of approximately 20-25 μg/dL produced increased auditory brainstem response thresholds in conjunction with morphological changes of the outer hair cells, including reduction in the tight junctions between endothelial and border cells [125]. Some of these studies indicated that such changes represented permanent effects of lead exposure [124].…”

Section: Do Attention Deficits And/or Hearing Loss Serve As Behavioramentioning

confidence: 99%

Developmental Exposure to Lead

Cory‐Slechta¹

2015

Environmental Factors in Neurodevelopmental and Neurodegenerative Disorders

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Lead exposure results in hearing loss and disruption of the cochlear blood–labyrinth barrier and the protective role of iron supplement

Cited by 34 publications

References 54 publications

Low Iron Diet Increases Susceptibility to Noise-Induced Hearing Loss in Young Rats

Low Iron Diet Increases Susceptibility to Noise-Induced Hearing Loss in Young Rats

Chronic lead exposure induces cochlear oxidative stress and potentiates noise-induced hearing loss

Developmental Exposure to Lead

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