In an article recently published in the journal Life Sciences, researchers studied the effect of nanosilver (Ag), noise, and nano-Ag plus noise treatments on rat cochlea. Research 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 auditory function and cochlear structure in male rats. Image Credit: JLRphotography/Shutterstock.com
A decrease in the percentage expression of TUJ-1 and MHC-7 proteins in rat cochlea was observed due to exposure to nano-Ag, noise, and nano-Ag plus noise, ultimately causing a deficit auditory at home.
Factors Causing Noise Induced Hearing Loss (NIHL)
Exposure to loud noise for an extended period of time can cause NIHL which damages cellular connections between cochlear cells, mixes perilymph and endolymph, and disrupts the synapse in primary spiral ganglion (SGN) neurons. Oxidative stress and reduced blood flow cause cochlear ischemia-reperfusion injury. Additionally, free radical generation and oxidative stress have been recognized as major causes of NIHL and cochlear dysfunction. During noise exposure, levels of lipid peroxidation are elevated, 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 the excessive release of cytokines. Ag NPs are widely used nanomaterials for industrial applications. Previous research has shown the toxicity of Ag-NPs leading to genotoxicity in cell lines and disrupting the cochlea. Combined exposure to nanomaterials and noise can provide reliable information on the expression of genes causing hearing loss. Moreover, this knowledge can help to develop new and robust molecular therapies or gene therapies.
Exposure of animal models to Ag-NPs and noise
In the present study, researchers synthesized Ag NPs and characterized them using SEM and XRD. They studied the nature of the 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 solution (PI), Ag NPs, 8 kilohertz narrowband noise, and a combination of noise and Ag NPs.
The team assessed changes in body weight, serum malondialdehyde (MDA) and superoxide dismutase (SOD) levels, and distortion product otoacoustic emissions (DPOAE). They stained rat cochlea to study mRNA expression, immunohistochemical (IHC) and histological alterations. Based on the research results, they confirmed the permanent damage to hair cells during subacute exposure to Ag NPs and noise.
For the first time, researchers reported that individual or concurrent exposure to noise and Ag-NPs contributed to biochemical alterations 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 concurrent effects resulted in damage to nerve and hair cells responsible for the perception of higher noise frequencies, resulting in permanent hearing loss.
Except in the noise plus Ag-NPs, they found that body weight in all groups had increased. However, compared to the control group, less weight gain was observed in the Ag-NPs plus noise group. These observations indicated that Ag-NPs and noise in combination are potent stressors that affect body weight.
The DPOAE test was used to assess the impact on OHCs and spiral ganglion (SGN) neurons, and the results revealed that DPOAE values were remarkably reduced in the noise-exposed groups. Combined exposure to Ag NPs and noise showed independent effects in the animal model. IHC results confirmed that co-exposure of animal models to noise and AG-NPs, in addition to hair cell loss, negatively impact SGNs. The combined exposure also resulted in the generation of ROS and an inflammatory response, as well as a decrease in SOD activity and an increase in serum MDA levels.
Moreover, the combined effect (Ag-NPs plus noise) increased the expression of NOX3, TNF and IL-6 in the animal groups. IHC testing revealed downregulation of beta-tubulin (TUJ1) and myosin-7a (MYO7A). The present study confirmed the role of the aforementioned genes and oxidative stress in the pathogenesis of Ag-NPs and noise, which induces auditory dysfunction and cochlear damage.
In conclusion, the researchers demonstrated that increased expression of MDA, IL-6, TNF-A, and NOX3 and decreased serum SOD levels, combined with molecular and functional data from Ag NPs and noise groups , caused inflammatory responses and oxidative stress damage to the cochlea.
Excess expression of genes (IL-6, TNF-A, NOX3), biochemical markers (SOD, MDA) and DPOAE assay revealed individual interactions of Ag NPs and noise. Additionally, histological changes in animal models exposed independently and combined to Ag NPs and noise revealed outer hair cell (OHC) and IHC counts.
Zahra, G., Esmaeil, K., Mohammad, F., Rashidy-Pour, A., Mahdi, M., Mahdi, A. and Ali, K. (2022). Combined effects of exposure to silver nanoparticles and noise on auditory function and cochlear structure in male rats. Life sciences. https://doi.org/10.1016/j.lfs.2022.120724