N-acetylcarnosine (NAC) drops for age-related cataract

Dubois, V.; Bastawrous, Andrew

doi:10.1002/14651858.cd009493.pub2

Cited by 25 publications

(30 citation statements)

References 15 publications

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“…Although cytotoxicity studies indicate that there is not a significant difference between the control NAC and SLN-NAC. This may be attributed to the fact that NAC has been previously regularly used as eye drops for treatment of cataract in a lot of studies [6–8]. Our work proves that SLN-NAC has even lower cell toxicity than NAC.…”

Section: Discussionsupporting

confidence: 67%

“…The Bode plot of the impediametric studies indicates an array of impedance pattern which yields typical pattern of least cell death (highest impedance values) in normal HENC cell line which is very similar to the SLN-NAC treated cells, followed by NAC treated cells. This typically indicates that the NAC is known to reduce the oxidative stress [8] and the synergistic effects of nanoparticles and NAC causes a membrane stabilizing effect and an antioxidant effect which tends to treat as well as reverse cataract. Corneal hydration is an integral part of study.…”

Section: Discussionmentioning

confidence: 99%

“…It is also known to have formed from oxidative stress. N-Acetyl Carnosine (NAC) is an ophthalmic drug which shows potential for treatment or even reversal of cataract [6–8]. A known antioxidant effect of the protein, L-carnosine, on cataractuous lens may allow us biochemically for exploring L-carnosine as a cause to converse or even avert development of cataract [9,10].…”

Section: Introductionmentioning

confidence: 99%

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An approach to revolutionize cataract treatment by enhancing drug probing through intraocular cell line

Liu

Huang

2018

Libyan Journal of Medicine

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The purpose of this study is to prepare and characterize solid lipid nanoparticles (SLN) of N-Acetyl Carnosine (NAC) to treat cataract since surgery necessitates equipments and professional help. Cataract is believed to be formed by the biochemical approach where the crystalline eye proteins lose solubility and forms high molecular weight masses. Added advantages of SLN of NAC (henceforth referred as SLN-NAC) in the study are reduced size, sustained release and better corneal penetration of drug. The method of preparation of SLN-NAC by Mill’s method is unique in itself.The size of the SLN-NAC was 75 ± 10 nm in the range of ideal for penetration. The in-vitro release study and the SLN-NAC formulations prepared with Mill’s method demonstrated sustained release up to 24 h following an initial burst after 1 h. The zeta potential of the prepared formulation was −22.1 ± 1 mV. Corneal permeation studies using goat corneas indicate that SLN-NAC penetration rate was higher than those from NAC eye drops. Corneal hydration studies indicated that the formulation caused no harm to the corneal cells.Therefore it may be concluded that SLN-NAC may revolutionize cataract treatment and reversal by improving drug permeation, reducing toxicity and no damage to corneal tissue.

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Section: Discussionsupporting

confidence: 67%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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An approach to revolutionize cataract treatment by enhancing drug probing through intraocular cell line

Liu

Huang

2018

Libyan Journal of Medicine

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“…It has been proposed that these age-related changes may reflect alterations in the ability to handle oxidative stress or alterations of the urea cycle in elderly compared to younger individuals (Chaleckis et al, 2016). N-acetyl carnosine has been formulated into eye drops to help ameliorate lipid peroxidation in the lens and treat cataracts (Babizhayev et al, 2014), although a recent Cochrane review failed to find convincing evidence of efficacy (Dubois and Bastawrous, 2017). These results are suggestive that people with RTT may have evidence of accelerated aging.…”

Section: Discussionmentioning

confidence: 99%

Metabolic Signatures Differentiate Rett Syndrome From Unaffected Siblings

Neul

Skinner

Annese

et al. 2020

Front. Integr. Neurosci.

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Rett syndrome (RTT, OMIM 312750), a severe neurodevelopmental disorder characterized by regression with loss of spoken language and hand skills, development of characteristic hand stereotypies, and gait dysfunction, is primarily caused by de novo mutations in the X-linked gene Methyl-CpG-binding protein 2 (MECP2). Currently, treatment options are limited to symptomatic management, however, reversal of disease phenotype is possible in mouse models by restoration of normal MECP2 gene expression. A significant challenge is the lack of biomarkers of disease state, disease severity, or treatment response. Using a non-targeted metabolomic approach we evaluated metabolite profiles in plasma from thirty-four people with RTT compared to thirty-seven unaffected age-and gender-matched siblings. We identified sixty-six significantly altered metabolites that cluster broadly into amino acid, nitrogen handling, and exogenous substance pathways. RTT disease metabolite and metabolic pathways abnormalities point to evidence of oxidative stress, mitochondrial dysfunction, and alterations in gut microflora. These observed changes provide insight into underlying pathological mechanisms and the foundation for biomarker discovery of disease severity biomarkers.

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“…Since the olfactory bulb is a gateway for external information and substances, carnosine is considered to be an endogenous neuroprotective substance, namely a 'neuroprotector' [15]. The supplement therapy of carnosine or its analogues are reportedly effective for the treatments of diabetes [16], cataract [17], and brain-related disorders such as depression and Gulf-war illness [18,19]. We have developed a system for quantitative analysis of carnosine using high-performance liquid chromatography (HPLC) [20] and demonstrated here the developmental changes of the amount of carnosine and its analogues in the brain.…”

Section: Introductionmentioning

confidence: 99%

Carnosine as a Possible Drug for Zinc-Induced Neurotoxicity and Vascular Dementia

Kawahara

Sadakane

Mizuno

et al. 2020

IJMS

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Increasing evidence suggests that the metal homeostasis is involved in the pathogenesis of various neurodegenerative diseases including senile type of dementia such as Alzheimer’s disease, dementia with Lewy bodies, and vascular dementia. In particular, synaptic Zn2+ is known to play critical roles in the pathogenesis of vascular dementia. In this article, we review the molecular pathways of Zn2+-induced neurotoxicity based on our and numerous other findings, and demonstrated the implications of the energy production pathway, the disruption of calcium homeostasis, the production of reactive oxygen species (ROS), the endoplasmic reticulum (ER)-stress pathway, and the stress-activated protein kinases/c-Jun amino-terminal kinases (SAPK/JNK) pathway. Furthermore, we have searched for substances that protect neurons from Zn2+-induced neurotoxicity among various agricultural products and determined carnosine (β-alanyl histidine) as a possible therapeutic agent for vascular dementia.

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N-acetylcarnosine (NAC) drops for age-related cataract

Cited by 25 publications

References 15 publications

An approach to revolutionize cataract treatment by enhancing drug probing through intraocular cell line

An approach to revolutionize cataract treatment by enhancing drug probing through intraocular cell line

Metabolic Signatures Differentiate Rett Syndrome From Unaffected Siblings

Carnosine as a Possible Drug for Zinc-Induced Neurotoxicity and Vascular Dementia

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