Implication of noise exposure on hearing with emphasis to hOGG1 and GPx-1 polymorphisms and HO-1 protein among textile workers

Abstract

Noise exposure is a health hazard in the textile industry. In cochlear hair cells, DNA damage caused by 8-oxoguanine (8-oxo G) can result in noise-induced hearing loss. Human 8-hydroxyguanine glycosylase (hOGG1) is a DNA repair enzyme that excises (8-oxo G) in the DNA and repairs DNA damage. Glutathione peroxidase-1 (GPx) is a crucial antioxidant enzyme that aids in limiting cochlear damages. Heme oxygenase-1 (HO-1) is a stress-inducible protein with a high fold change in the hair cells of the cochlea. The study aimed to investigate the association of either hOGG1 and GPx-1 polymorphisms with audiometric notches and HO-1 protein among textile workers. hOGG1 and GPx genotypes were analyzed by PCR–RFLP, and HO-1 levels were measured by ELISA in 115 male textile workers. Blood pressure and audiogram were performed. Results recorded the relation between audiometric notches and ear complaints among workers. Older age workers showed audiometric notches at > 25 dB with a significant decrease in HO-1 levels and higher levels in workers with normal audiogram. Ser/Cys genotype of hOGG1 gene was associated with age and work duration while CC genotype of GPx is associated with HO-1 levels and diastolic pressure. Ser/Cys genotype of hOGG1 gene was associated with age while Cys/Cys genotype was associated with work duration among workers. CC genotype of GPx gene was associated with higher HO-1 levels and TT genotype was associated with high diastolic pressure. Finally, hearing impairment was dependent on the duration of exposure to noise, older age, and the presence of heterozygote TC genotype of GPx gene among textile workers.

The miR-182-5p/GPX4 Pathway Contributes to Sevoflurane-Induced Ototoxicity via Ferroptosis

“…Another study showed that sevoflurane caused mitochondrial ROS production and elevated cytoplasmic calcium levels, triggering the opening of the mitochondrial permeability transition pore (MPTP) and lowering the mitochondrial membrane potential (MMP), inducing mitochondrial iron overload, and ultimately leading to cognitive dysfunction [ 31 ]. The peripheral auditory nervous system is similarly susceptible to damage by drugs and the environment [ 7 , 32 , 33 ]. Our previous study showed that sevoflurane was capable of producing ototoxicity in the developing peripheral auditory system by inducing oxidative stress [ 9 ].…”