What Supplements and Vitamins Are Best for Protecting Your Ears and Keeping Your Hearing Threshold?
- Thread starter IvanRus
- Start date
- Feb 17, 2017
- 10,400
- Tinnitus Since
- February, 2017
- Cause of Tinnitus
- Acoustic Trauma
TuneOut
Member
Free radicals are generated during excessive sound exposure and do damage to the ears. Many antioxidants are likely to provide some protection by quenching these destructive molecules.
Acetyl-L-Carnitine (ALCAR), as you mention, has been shown to provide some protection from acoustic trauma. Note that in the following study outer hair cell (OHC) loss was reduced by 80%.
Pharmacological rescue of noise induced hearing loss using N-acetylcysteine and acetyl-L-carnitine.
Coleman JK, et al. Hear Res. 2007.
"The capacity for ALCAR to reduce the damaging effects of noise-induced cochlear stress was hypothesized to occur through its effects on bioenergetics and biogenesis of the mitochondrion. Seidman et al. (2000) demonstrated in rats that age-related hearing loss, which is also associated with cochlear oxidative stress, was attenuated by ALCAR administration. Kopke et al. (2002, 2005) observed that PTS and HC loss were significantly reduced in their chinchilla model when ALCAR was delivered systemically prior to and just after both continuous and impulse noise. As demonstrated in the current study, ALCAR effectively decreased PTS additionally an average of 17.9 dB SPL for the 1-h and 15.4 dB SPL for the 4-h post-treatment groups compared to the saline, noise exposed animals. OHC and IHC loss was also 80% and 55%, and 24% and 23% less, respectively, for the 1 and 4 h post-treatment groups.
There is increasing evidence that during oxidative stress, mitochondria produce more superoxide anions injuring the mitochondria. The injured mitochondria in turn produce relatively more ROS further accentuating the damage
(Lenaz et al., 1998; Poderoso et al., 2000). Mitochondrial injury is a critical factor in NIHL resulting from excessive
ROS generation within mitochondria or from glutamate excitotoxicity or GSH depletion (Hyde and Rubel, 1995;
Kroemer, 1999; Kroemer and Reed, 2000; Kopke et al., 2002; Coling et al., 2003; Fischel-Ghodsian et al., 2004). It is suggested that ALCAR protect mitochondria from oxidative stress by maintaining normal electron transport and reducing ROS production by way of its effects on the mitochondrial membrane. ALCAR has scavenging effects on the superoxide anion and increases reduced glutathione and coenzymeQ10, thereby decreasing membrane lipid peroxidation. As suggested by electron microscopic analysis, ALCAR provided protection against mitochondrial damage by maintaining morphological and structural integrity of inner and outer mitochondrial membranes (Fig. 5A–C), and mitochondrial density and number (Fig. 6A and B) compared to saline treated, noise-exposed animals three weeks post-noise exposure."
There is increasing evidence that during oxidative stress, mitochondria produce more superoxide anions injuring the mitochondria. The injured mitochondria in turn produce relatively more ROS further accentuating the damage
(Lenaz et al., 1998; Poderoso et al., 2000). Mitochondrial injury is a critical factor in NIHL resulting from excessive
ROS generation within mitochondria or from glutamate excitotoxicity or GSH depletion (Hyde and Rubel, 1995;
Kroemer, 1999; Kroemer and Reed, 2000; Kopke et al., 2002; Coling et al., 2003; Fischel-Ghodsian et al., 2004). It is suggested that ALCAR protect mitochondria from oxidative stress by maintaining normal electron transport and reducing ROS production by way of its effects on the mitochondrial membrane. ALCAR has scavenging effects on the superoxide anion and increases reduced glutathione and coenzymeQ10, thereby decreasing membrane lipid peroxidation. As suggested by electron microscopic analysis, ALCAR provided protection against mitochondrial damage by maintaining morphological and structural integrity of inner and outer mitochondrial membranes (Fig. 5A–C), and mitochondrial density and number (Fig. 6A and B) compared to saline treated, noise-exposed animals three weeks post-noise exposure."
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