In a recently published article in the magazine life sciences, researchers examined the effect of nanosilver (Ag), noise and nano-Ag plus noise treatments on the cochlea of rats. The study results confirmed that these treatments induced oxidative stress in rats and altered the expression of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), and NADPH oxidase 3 (NOX3).
Study: Combined effects of exposure to silver nanoparticles and noise on the hearing function and cochlear structure of the male rats† Image Credit: JLRphotography/Shutterstock.com
A decrease in the expression rate of TUJ-1 and MHC-7 proteins in the cochlea of rats was observed due to exposure to nano-Ag, noise and nano-Ag plus noise, ultimately leading to a hearing loss in them.
Factors that cause noise-induced hearing loss (NIHL)
Exposure to intense noise over an extended period of time can cause NIHL that damages the cellular connections between cochlear cells, mixes the perilymph and endolymph, and disrupts the synapse in primary spiral ganglion neurons (SGNs). Oxidative stress and decreased blood flow cause cochlear ischemia-reperfusion damage. In addition, free radical formation and oxidative stress were recognized as the major causes of NIHL and cochlear dysfunction. When exposed to sound, levels of lipid peroxidation are increased, leading to increased production of free radicals in the cochlea.
Metal nanoparticles (NPs) mainly cause toxicity via the production of reactive oxygen species (ROS) and excessive release of cytokines. Ag NPs have widely used nanomaterials for industrial applications. Previous research showed that the toxicity of Ag-NPs leads to genotoxicity in cell lines and disrupts the cochlea. The combined exposure to nanomaterials and sound can provide reliable information about gene expression that causes hearing loss. In addition, this knowledge can help build new and robust molecular therapies or gene therapy.
Exposure of animal models to Ag-NPs and noise
In the present study, the researchers synthesized Ag NPs and characterized them using SEM and XRD. They investigated the nature of interactions (independent, additive or synergistic) displayed by the integrated exposure of an animal model to Ag-NPs and intensive noise. The researchers divided 24 Wistar rats into four treatment groups and were exposed to saline (IP), Ag NPs, 8 kilohertz narrowband noise, and a combination of noise and Ag NPs.
The team assessed changes in body weight, levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in serum, and otoacoustic emissions of deformation products (DPOAE). They stained the rat cochlea to examine mRNA expression, immunohistochemical (IHC), and histological changes. Based on the study results, they confirmed the permanent damage to hair cells upon subacute exposure to Ag NPs and noise.
For the first time, the researchers reported that individual or concomitant exposure to noise and Ag-NPs contributes to biochemical changes in serum, morphological, functional and IHC changes in rat cochlear cells. The present study provided in vivo evidence on the negative effects of noise and Ag-NPs on cochlear cells. These simultaneous effects resulted in damage to nerve and hair cells, which are responsible for perceiving higher sound frequencies, resulting in permanent hearing loss.
Except in noise plus Ag-NPs, they found body weight increased in all groups. However, compared to the control group, a smaller weight gain was observed in the Ag-NPs plus the noise group. These observations indicated that the Ag-NPs and noise in combination are strong stressors that affect body weight.
The DPOAE test helped assess the impact on OHCs and spiral ganglion neurons (SGNs), and the results showed that DPOAE levels were markedly reduced in the noise-exposed groups. The combined exposure to Ag NPs and noise showed independent effects on the animal model. The IHC results confirmed that the simultaneous exposure of animal models to noise and AG-NPs in addition to hair cell loss negatively impacted SGNs. The combined exposure also led to ROS generation and inflammatory response, along with decreased SOD activity and increased serum MDA levels.
In addition, the combined effect (Ag-NPs plus noise) increased the expression of NOX3, TNF and IL-6 in the animal groups. The IHC tests revealed downregulation of beta tubulin (TUJ1) and myosin-7a (MYO7A). The present study confirmed the role of the above genes and oxidative stress in the pathogenesis of Ag-NPs and noise, which caused hearing impairment and cochlear damage.
In conclusion, the researchers showed that increased expression of MDA, IL-6, TNF-A and NOX3 and decreased serum SOD levels combined with molecular and functional data from the Ag NPs and noise groups resulted in inflammatory responses and oxidative stress damage to the cochlea.
The overexpression of genes (IL-6, TNF-A, NOX3), biochemical markers (SOD, MDA) and the DPOAE assay revealed individual interactions of Ag NPs and noise. Furthermore, histological changes in the animal models independently exposed and combined with Ag NPs and noise revealed the number of outer hair cells (OHCs) and IHCs.
Zahra, G., Esmaeil, K., Mohammad, F., Rashidy-Pour, A., Mahdi, M., Mahdi, A., & Ali, K. (2022). Combined effects of exposure to silver nanoparticles and noise on the hearing function and cochlear structure of the male rats. life sciences† https://doi.org/10.1016/j.lfs.2022.120724
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