• YAKHAK HOEJI
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• v.54 no.5
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• pp.334-340
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• 2010

We investigated whether poly-L-histidine (PLH) significantly affect mucin release from cultured airway epithelial cells. Confluent primary hamster tracheal surface epithelial (HTSE) cells were metabolically radiolabeled with $^$^3H$$glucosamine for 24 hr and chased for 30 min in the presence of PLH to assess the effect on $^3H$-mucin release. PLH 9,850 and PLH 6,700 specifically inhibit mucin release from airway goblet cells without significant cytotoxicity. This finding suggests that poly-L-histidine might function as an airway mucoregulative agent.

• Bulletin of the Korean Chemical Society
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• v.15 no.8
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• pp.673-679
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• 1994

$^1H$ NMR spectra of imidazole, 2-and 4(5)-methylimidazole, histamine, L-histidine, L-histidine methyl ester, N${\alpha}$-acetyl-L-histidine, and L-carnosine coordinated to the paramagnetic undecatungstocobalto(II)silicate ($SiW_{11}Co$) and undecatungstonickelo(II)silicate ($SiW_{11}Ni$) anions are reported. For these complexes the ligand exchange is slow on the NMR time scale and the pure resonance lines of the free ligand and the complexes have been observed separately at room temperature. Two different complexes are formed, depending upon which nitrogen atom of the imidazole ring is coordinated to the cobalt or nickel ion of $SiW_{11}M$. Thus the NMR spectrum of a $D_2O$ solution containing a ligand and $SiW_{11}M$ consists of three sets of lines originating from the free ligand and two complexes. All NMR lines of the $SiW_{11}Co$ complexes have been assigned unequivocally using the saturation transfer technique. The temperature dependence of some spectra are also reported. The NMR spectra of some complexes show that the internal rotation of the substituent on the imidazole ring is hampered by the heteropolyanion moiety even at room temperature.

• Nutrition Research and Practice
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• v.8 no.1
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• pp.3-10
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• 2014

The rapid increase in the prevalence of metabolic syndrome, which is associated with a state of elevated systemic oxidative stress and inflammation, is expected to cause future increases in the prevalence of diabetes and cardiovascular diseases. Oxidation of polyunsaturated fatty acids and sugars produces reactive carbonyl species, which, due to their electrophilic nature, react with the nucleophilic sites of certain amino acids. This leads to formation of protein adducts such as advanced glycoxidation/lipoxidation end products (AGEs/ALEs), resulting in cellular dysfunction. Therefore, an effective reactive carbonyl species and AGEs/ALEs sequestering agent may be able to prevent such cellular dysfunction. There is accumulating evidence that histidine containing dipeptides such as carnosine (${\beta}$-alanyl-L-histidine) and anserine (${\beta}$-alanyl-methyl-L-histidine) detoxify cytotoxic reactive carbonyls by forming unreactive adducts and are able to reverse glycated protein. In this review, 1) reaction mechanism of oxidative stress and certain chronic diseases, 2) interrelation between oxidative stress and inflammation, 3) effective reactive carbonyl species and AGEs/ALEs sequestering actions of histidine-dipeptides and their metabolism, 4) effects of carnosinase encoding gene on the effectiveness of histidine-dipeptides, and 5) protective effects of histidine-dipeptides against progression of metabolic syndrome are discussed. Overall, this review highlights the potential beneficial effects of histidine-dipeptides against metabolic syndrome. Randomized controlled human studies may provide essential information regarding whether histidine-dipeptides attenuate metabolic syndrome in humans.

• Journal of Aquaculture
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• v.20 no.1
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• pp.19-25
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• 2007

For establishing a basal diet for the Pacific bluefin tuna Thunnus orientalis (PBT), feeding stimulants were initially identified by omission test using the synthetic extract of horse mackerel, Trachurus japonicus. Four feeding trials were conducted using juvenile PBT weighing $9.0{\pm}0.91\;g$ (trial 1, 2 and 3) and $1.6{\pm}0.23\;g$ (trial 4), which were originated from an artificial seedling production. The fish fed the casein diet with each test solution were added at the ratio of 100 g casein diet to 100 g jack mackerel muscle. A complete synthetic extract of jack mackerel containing all 3 fractions, amino acid, nucleotide and organic nitrogenous base, exhibited a comparable feeding stimulant activity compared to that of natural extract. The omission of nucleotide or amino acid fraction showed lower feeding activity, but the omission of other nitrogenous fraction maintained a similar feeding stimulant activity compared to that of the synthetic extract (trial 1). Inosine-5' monophosphate $Na_2$ (IMP) was identified as a major constituent for maintaining feeding activity. The mixture of L-alanine, L-glutamic acid, L-histidine, L-lysine, taurine and IMP induced a similar feeding activity compared to that of the synthetic extract (trial 2 and 3). In trial 4, the highest feeding activity was finally obtained in the mixture of L-histidine, L-glutamine and IMP, followed by the synthetic extract, the mixture of L-lysine, L-alanine and IMP, IMP and the mixture of L-histidine, L-glutamic acid, L-lysine and L-alanine. These results revealed that the mixture of L-histidine, L-glutamic acid and IMP for the proper feeding stimulant of PBT in this study.

• Animal Bioscience
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• v.37 no.11
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• pp.1834-1847
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• 2024

Objective: The effects of carnosine synthesis on the structural and microstructural determinants of meat quality have not been studied to date. Therefore, this study aimed to investigate the effect of supplementation with carnosine synthesis precursors on the characteristics and microstructure of breast muscle fibers in slow-growing Korat chickens (KR). Methods: Slow-growing KR were fed a non-supplemented commercial diet (control group) or a commercial diet supplemented with 1.0% β-alanine, 0.5% L-histidine, or a combination of both 1.0% β-alanine and 0.5% L-histidine. At 10 weeks, KR were slaughtered, and the breast muscle was collected. Samples were fixed and extracted to study the microstructure, fat level, and porosity of the meat using X-ray and scanning electron microscopy, and real-time polymerase chain reaction was performed to analyze the expression of genes related to myofiber differentiation. Results: L-histidine supplementation significantly altered myofiber diameter and muscle fiber density and compactness by regulating muscle fiber-type differentiation via carnosine synthase (CARNS1) and myocyte enhancer factor 2C expression, as well as myogenic differentiation antigen and myogenic regulatory factor 5 expression. While excess L-histidine potentially stimulated CARNS1 to modify muscle fiber arrangement and tenderness in breast meat, dietary β-alanine supplementation alone or in combination with L-histidine supplementation induced a relatively less remarkable but not significant (p<0.05) effect on the breast meat characteristics studied. Conclusion: Interestingly, the combination of β-alanine and L-histidine supplementation had no effect on meat microstructure, meat porosity, and fat content in comparison with the control group. Thus, this combination had the best selectivity for improving meat quality. However, further studies are required to clarify the effects of carnosine levels on meat processing.

• Journal of Microbiology and Biotechnology
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• v.9 no.5
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• pp.613-618
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• 1999

L-Proline-producing mutant strains were developed by exposing L-glutamic acid-producing bacteria to N-metyl-N-nitro-nitrosoguanidine and UV irradiation. A L-histidine auxotroph of Corynebacterium acetoacidophilum RYU3161(KCTC 0616BP), which was resistant to sulfaguanidine and proline analogs (DHP, AZC, TAC), was isolated. The activity of the mutant strain's $\gamma$-glutamyl kinase was 45% higher than that of the parent strain. The optimum level of L-histidine for production of L-proline was 0.16 g/l. In a 5-1 jar fermenter, the mutant strain produced L-proline at a high concentration (35 g/l) level within 48 h of cultivation.

• Journal of the Korean Society of Food Science and Nutrition
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• v.34 no.5
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• pp.681-686
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• 2005

The purpose of this study was to analyze the chemical component of Camellia japonica L. according to picking time. Leaves of Camellia japonica L. were picked in April and May,2003. Free sugars (fructose, glucose and sucrose) and organic acids (citric acid, tartaric acid, succinic acid, acetic acid) were present in the Camellia japonica L. leaf. The contents of total free sugars and organic acids increased as picking time was delayed. The major components of free amino acids were aspartic acid, glutamic acid and histidine, and those of total amino acids were histidine and alanine. The contents of total free amino acids and total amino acids were decreased as picking time was delayed, while the ratio of essential amino acids to the total amino acids increased. The amount of minerals (P, Ca, K, Na and Fe), chlorophyll and total polyphenol increased as picking time was delayed.

• Bulletin of the Korean Chemical Society
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• v.29 no.8
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• pp.1539-1544
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• 2008

A polymeric micelle, based on the poly(benzyl-L-histidine)-b-poly(ethylene glycol) (polyBz-His-b-PEG) diblock copolymer, was designed as a tumor-specific targeting carrier. The micelles (particle size: 67-80 nm, critical micelle concentration (CMC); 2-3 $\mu$g/mL) were formed from the diafilteration method at pH 7.4, as a result of self-assembly of the polyBz-His block at the core and PEG block on the shell. Removing benzyl (Bz) group from polyBz-His block provided pH-sensitivity of the micellar core; the micelles were physically destabilized in the pH range of pH 7.4-5.5, depending on the content of the His group free from Bz group. The ionization of His group at a slightly acidic pH promoted the deformation of the interior core. These pHdependent physical changes of the micelles provide the mechanism for pH-triggering anticancer drug (e.g., doxorubicin: DOX) release from the micelle in response to the tumor’s extracellular pH range (pH 7.2-6.5).

• Journal of Microbiology and Biotechnology
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• v.11 no.5
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• pp.838-844
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• 2001

The enzyme Fuc aldolase from Methanococcus jannaschii that catalyzes the aldol condensation of DHAP and L-lactaldehyde to give fuculose-1-phosphate was inactivated by DEP. The inactivation was pseudo first-order in the enzyme and DEP, which was biphasic. A pseudo second-order rate constant of 120$M^{-1}min^{-1}$ was obtained at pH 6.0 and $25{\circ}C$. Quantifying the increase in absorbance at 240nm showed that four histidine residues per subunit were modified during the nearly complete inactivation. The statistical analysis and the time course of the modification suggested that two or three histidine residues were essential for activity. The rate of inactivation was dependent on the pH, and the pH inactivation data implied the involvement of the amino acid residue with a $pK_a$ value of 5.7. Fuc aldolase was protected against DEP inactivation by DHAP, indicating that the histidine residues were located at the active site of Fuc aldolase. DL-Glyceraldehyde, as an alternative substrate to L-lactaldehyde, showed no specific protection for the Fuc aldolase.

• Journal of Microbiology and Biotechnology
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• v.30 no.2
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• pp.306-312
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• 2020

Despite the importance of brown adipocytes as a therapeutic target for the prevention and treatment of obesity, the molecular mechanism underlying brown adipocyte differentiation is not fully understood. In particular, the role of post-translational modifications in brown adipocyte differentiation has not been extensively studied. Histidine phosphorylation is increasingly recognized an important process for protein post-translational modifications. In this study, we show that histidine phosphorylation patterns change during brown adipocyte differentiation. In addition, the expression level of protein histidine phosphatase 1 (PHPT1), a major mammalian phosphohistidine phosphatase, is reduced rapidly at the early phase of differentiation and recovers at the later phase. During white adipocyte differentiation of 3T3-L1 preadipocytes, however, the expression level of PHPT1 do not significantly change. Knockdown of PHPT1 promotes brown adipocyte differentiation, whereas ectopic expression of PHPT1 suppresses brown adipocyte differentiation. These results collectively suggest that histidine phosphorylation is closely linked to brown adipocyte differentiation and could be a therapeutic target for obesity and related metabolic diseases.