N-Acetyl-L-tyrosine

N-acetyl-L-Tyrosine (NAT) is an active metabolite of, and precursor to, L-tyrosine.^1,2 Dietary administration of NAT increases B. mori larvae heat stress tolerance and A. mellifera survival in a model of environmental stress.² Blood levels of NAT are increased during heat and restraint stress in mice, and dietary administration of NAT decreases blood lipid peroxidation and corticosterone levels in a mouse model of restraint stress. Dietary administration of NAT also decreases tumor volume in an HCT116 mouse xenograft model. Urinary excretion of NAT is increased in patients with phenylketonuria (PKU) or tyrosinemia, inborn errors of amino acid metabolism characterized by mutations in the gene encoding phenylalanine hydroxylase (PAH) and a deficiency in fumarylacetoacetate hydrolase (FAH), the final enzyme in tyrosine catabolism, respectively.¹ Formulations containing NAT have been used for amino acid supplementation in parenteral nutrition for preterm infants.

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1. Jellum, E., Horn, L., Thoresen, O., et al. Urinary excretion of N-acetyl amino acids in patients with some inborn errors of amino acid metabolism. Scand. J. Clin. Lab. Invest. Suppl. 184, 21-26 (1986).

2. Matsumura, T., Uryu, O., Matsuhisa, F., et al. N-acetyl-L-tyrosine is an intrinsic triggering factor of mitohormesis in stressed animals. EMBO Rep. 21(5), e49211 (2020).