• Food Science of Animal Resources
• /
• v.39 no.5
• /
• pp.704-724
• /
• 2019

This study mainly investigated the improvement effect of nitroso-hemoglobin (NO-Hb) and four lactic acid bacteria (LAB) (Streptococcus thermophiles, Lactobacillus bulgaricus, Lactobacillus casei, and Montessori enterococcus) on the color and microbiological qualities of raw beef. Three strains of Escherichia coli, Staphylococcus, Salmonella, and Pseudomonas were used as pathogenic bacteria. The results showed that both NO-Hb and LAB could enhance the color stability and scavenged the spoilage bacteria in a minced beef model. But the improvement effect of NO-Hb was more significant than LAB. This suggested that NO-Hb, as a novel ingredient, could be used as a promising substitute for nitrite in meat products to improve the color and safety of meat products. In addition, low field (LF)-NMR method has been established to be practicable to identify changes in the relaxation times of water and fat caused by different type of bacteria and the storage periods. The number of relaxation components in minced beef was affected by bacteria and increase of the storage period.

• The Korean Journal of Physiology and Pharmacology
• /
• v.1 no.6
• /
• pp.673-679
• /
• 1997

It has been generally accepted that glutamate mediates the ischemic brain damage, excitotoxicity, and induces release of neurotransmitters, including norepinephrine(NE), in ischemic milieu. In the present study, the role of nitric oxide(NO) in the ischemia-induced $[^3H]norepinephrine([^3H]NE)$ release from cortex slices of the rat was examined. Ischemia, deprivation of oxygen and glucose from $Mg^{2+}-free$ artificial cerebrospinal fluid, induced significant release of $[^3H]NE$ from cortex slices. This ischemia-induced $[^3H]NE$ release was significantly attenuated by glutamatergic neurotransmission modifiers. $N^G-nitro-L-arginine$ methyl ester(L-NAME), $N^G-monomethyl-L-arginine$ (L-NMMA) or 7-nitroindazole, nitric oxide synthase inhibitors attenuated the ischemia-evoked $[^3H]NE$ release. Hemoglobin, a NO chelator, and 5, 5- dimethyl-L-pyrroline-N-oxide(DMPO), an electron spin trap, inhibited $[^3H]NE$ release dose-dependently. Ischemia-evoked $[^3H]NE$ release was inhibited by methylene blue, a soluble guanylate cyclase inhibitor, and potentiated by 8-bromo-cGMP, a cell permeable cGMP analog, zaprinast, a cGMP phosphodiesterase inhibitor, and S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide generator. These results suggest that the ischemia-evoked $[^3H]NE$ release is mediated by NMDA receptors, and activation of NO system is involved.