Neomycine is not like what you had written.

Neomycin belongs to the aminoglycoside family of antibiotics. The group is known for their 3 toxicities e.g., ototoxic, nephrotoxic and neurotoxic. Thus it is used only topically in clinical practice and orally in some cases.

One explanation, for instance regarding ototoxicity, is the genetic predisposition of the hairy cell mitochondria. The excerpt below is from Huth et al. 2011 https://www.hindawi.com/journals/ijoto/2011/937861/

"...One main susceptibility factor (17%–33% of patients with reported ototoxic damage [61]) is the genetic predisposition to AG ototoxicity [62]. The fact that this increased susceptibility was inherited maternally suggested mitochondrial involvement [62]. This is compelling in light of the endosymbiotic theory as mitochondrial ribosomes demonstrate more similarities to prokaryotic ribosomes than cytosolic ribosomes [63, 64]. Therefore, the small subunit of the mitochondrial ribosome is one of the primary targeting sites for AGs [48, 49].

Several mutations in mitochondrial DNA are linked to increased susceptibility to AG ototoxicity [61, 65, 66]. Exposure to AG leads to impairment of RNA translation within mitochondria through interaction with binding sites on mitochondrial 12S rRNA [65]. This interaction was mapped to an adenine-to-guanine mutation at nucleotide 1555 in the 12S rRNA gene [65]. Of additional note, bacterial resistance mutations are described at this locus [67, 68]. This mutation increases structural similarity of mitochondrial rRNA to bacterial rRNA [65], which promotes binding of AG to mutated mitochondrial 12S rRNA [69, 70]. As a result, damage can result from decreased protein synthesis [69]. Although no direct evidence exists to link ototoxicity to an inhibition of mitochondrial protein synthesis, inhibition of mitochondrial protein synthesis potentiates AG toxicity [71]. Also, electron microscopy reveals mitochondrial disruption following AG treatment [72].

This susceptibility mutation has been reported in 17%–33% of patient with reported AG ototoxicity [61]; in the general population of the European Union, it is estimated to be 1 : 500 [73, 74]. Other mutations leading to increased AG susceptibility have also been described, including C1494T [66]. The C1494T mutations have varying degrees of penetrance [75], are less common than the A1555G mutation [76], and are sporadic with multiple origins [77]. In sum, the prevalence of the most common mutations across varying ethnic backgrounds is 0.9%–1.8% [76, 78], of which 5%-6% are sporadic [63, 79, 80]...."

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