Differential ototoxicities induced by lead acetate and tetraethyl lead

Tuncel, Ümit; Clerici, William J.; Jones, Raleigh O.

doi:10.1016/s0378-5955(02)00303-9

Cited by 16 publications

(6 citation statements)

References 75 publications

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“…Other animal studies also found no significant Pb-related effects on the cochlea. Experimental studies using guinea pigs exposed to Pb, or in vitro experiments on dissociated guinea pig outer hair cells bathed in Pb acetate found no apparent morphological changes in the cochlea, no marked effects on the endocochlear potential or the cochlear microphonic response, and no significant effects on outer hair cell electromotility (the process leading to the generation of otoacoustic emissions) (Gozdzik-Zolnierkiewicz & Moszynski, 1969; Yamamura, et al, 1989; Tuncel, et al, 2002; Liang et al, 2004). Because the cochlear microphonic response (or receptor potential) is generated primarily by the outer hair cells of the inner ear, ototoxic effects should be manifested in both a diminished cochlear microphonic response and abnormal DPOAE, although DPOAE may be more hair cell place-specific than the cochlear microphonic.…”

Section: Discussionmentioning

confidence: 97%

Environmental Lead Exposure and Otoacoustic Emissions in Andean Children

Buchanan

Counter

Ortega

2011

Journal of Toxicology and Environmental Health, Part A

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Studies relating sensory hearing impairment to lead (Pb) exposure in children have presented inconsistent results. The objective of this study was to measure distortion product otoacoustic emissions (DPOAE), sounds emanating from the outer hair cells of the inner ear, in Pb-exposed children to determine the effects of Pb poisoning on the inner ear. DPOAE were recorded for 9 f2 frequencies from 1187 to 7625 Hz on 102 ears of 53 Pb-exposed children (aged 6–16 years) residing in Pb-contaminated environments in the Andes Mountains of Ecuador where Pb-glazing of ceramics is the primary livelihood. Blood lead (PbB) levels ranged from 4.2 to 94.3 µg/dl (mean: 37.7; SD: 25.7; median: 36.4). The median PbB level was significantly higher than the CDC and WHO’s 10 µg/dl action level. Spearman rho correlation analyses of the relation between PbB level and DPOAE amplitude, and between PbB level and DPOAE signal-to-noise ratio revealed no significant associations at any of the f2 frequencies tested. In addition, no significant correlation (Spearman rho) between PbB level and hearing sensitivity for 6 pure-tone test frequencies from 1000–8000 Hz was found. Although the study group was found to have abnormally elevated PbB levels, in contrast to some earlier reports, the results of the current study showed no consistent Pb-induced sensory effects on the cochlea of Pb-intoxicated children.

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Section: Discussionmentioning

confidence: 97%

Environmental Lead Exposure and Otoacoustic Emissions in Andean Children

Buchanan

Counter

Ortega

2011

Journal of Toxicology and Environmental Health, Part A

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“…Lead has also been implicated as a potential ototoxicant in developing animals, including mice (Jones et al 2008; Fortune and Lurie 2009; Prins et al 2010) and monkeys (Rice 1997) and acute Pb exposures may generate auditory dysfunction in guinea pigs (Tuncel et al 2002). Similarly, Cd in drinking water at 5, 15, or 150 ppm produced ototoxic effects in 30-day exposures in two rat and one mouse study (Ozcaglar et al 2001; Agirdir et al 2002; Kim et al 2008).…”

Section: Introductionmentioning

confidence: 99%

Assessing ototoxicity due to chronic lead and cadmium intake with and without noise exposure in the mature mouse

Carlson

Schacht

Neitzel

2018

Journal of Toxicology and Environmental Health, Part A

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Exposure to heavy metals may lead to hearing impairment. However, experimental studies have not explored this issue with and without noise exposure in mature animals with environmentally relevant doses. The aim of this study was to investigate ototoxicity produced by lead (Pb) and cadmium (Cd) and noise, singly and in combination, in the adult CBA/CaJ mouse. Metals were delivered via drinking water (0.03 mM, 1 mM, and 3 mM Pb; or 30, 100, and 300 μM Cd) for 12 weeks, resulting in environmentally- and occupationally-relevant mean (± standard deviations) blood levels of Pb (2.89 ± 0.44, 38.5 ± 4.9, and 60.1 ± 6.6 μg/dl, respectively) and Cd (1.3 ± 0.23, 6.37 ± 0.87, 27.2 ± 4.1 μg/L, respectively). Metal treatment was also combined with a noise exposure consisting of a 105 dB broadband (2–20 kHz) stimulus for 2 hr or a sham exposure. Auditory performance was determined by comparing auditory brainstem responses (ABR) and otoacoustic emissions (DPOAE) at baseline and after 11 weeks of metal treatment. Metal-exposed animals did not develop significant auditory deficits and did not exhibit morphological damage to cochlear hair cells. In contrast, noise-exposed animals, including those exposed to combinations of metals and noise, demonstrated significant hair cell loss, reduced DPOAE amplitudes, and ABR threshold shifts of 42.2 ± 13 dB at 32 kHz (105 dB noise alone). No significant potentiation or synergistic effects were found in groups exposed to multiple agents. This study establishes a highly reproducible adult mouse model that may be used to evaluate a variety of environmental exposure mixtures.

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“…One of the major environmental concerns throughout the world is the exposure to tetraethyl lead (Tuncel et al 2002). Tetraethyl lead is an organic compound used as a gasoline additive because of its anti-knocking properties (Venkateswarw et al 2003), but exposure to this compound causes health hazards.…”

Section: Introductionmentioning

confidence: 99%

Exposure to 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin and tetraethyl lead affects lung mitochondria bioenergetics

Simões

Duarte

Rolo

et al. 2010

Toxicology Mechanisms and Methods

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Environmental pollutants such as TCDD and tetraethyl lead are extremely toxic and related with pulmonary disease development. Lung mitochondria are primary cellular targets for dioxins exposure-induced toxicity. TCDD showed a delay in the repolarization after a phosphorylative cycle and a decrease on state 3 respiration, suggesting alterations at the phosphorylative system level. The ATPase activity showed no differences between control and lung mitochondria incubated with TCDD, implying alterations in other components of the phosphorylative system. Tetraethyl lead also showed a delay in the repolarization after a phosphorylative cycle and a decrease on RCR. These data suggest that lung mitochondria incubated with TCDD and tetraethyl lead showed impaired mitochondrial function, reflecting the loss of oxidative phosphorylation capacity.

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Differential ototoxicities induced by lead acetate and tetraethyl lead

Cited by 16 publications

References 75 publications

Environmental Lead Exposure and Otoacoustic Emissions in Andean Children

Environmental Lead Exposure and Otoacoustic Emissions in Andean Children

Assessing ototoxicity due to chronic lead and cadmium intake with and without noise exposure in the mature mouse

Exposure to 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin and tetraethyl lead affects lung mitochondria bioenergetics

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