scholarly journals Comparison of glucose, lactate, and nucleotide degradation products content of cooked Hanwoo and Australian beef steaks by internal temperature

2015 ◽  
Vol 42 (4) ◽  
pp. 369-374
Author(s):  
Sun-Moon Kang ◽  
Geun-Ho Kang ◽  
Pil-Nam Seong ◽  
Young-Chun Kim ◽  
Jin-Hyoung Kim ◽  
...  
Keyword(s):  
Degradation Products ◽  
Internal Temperature ◽  
Beef Steaks ◽  
Nucleotide Degradation

scholarly journals Increased Adenine Nucleotide Degradation in Skeletal Muscle Atrophy

2019 ◽  
Vol 21 (1) ◽  
pp. 88 ◽  
Author(s):  
Spencer G. Miller ◽  
Paul S. Hafen ◽  
Jeffrey J. Brault
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Intracellular Signaling ◽  
Adenine Nucleotide ◽  
Degradation Products ◽  
Adenine Nucleotides ◽  
Skeletal Muscle Atrophy ◽  
Valuable Insight ◽  
Disease States ◽  
Nucleotide Degradation

Adenine nucleotides (AdNs: ATP, ADP, AMP) are essential biological compounds that facilitate many necessary cellular processes by providing chemical energy, mediating intracellular signaling, and regulating protein metabolism and solubilization. A dramatic reduction in total AdNs is observed in atrophic skeletal muscle across numerous disease states and conditions, such as cancer, diabetes, chronic kidney disease, heart failure, COPD, sepsis, muscular dystrophy, denervation, disuse, and sarcopenia. The reduced AdNs in atrophic skeletal muscle are accompanied by increased expression/activities of AdN degrading enzymes and the accumulation of degradation products (IMP, hypoxanthine, xanthine, uric acid), suggesting that the lower AdN content is largely the result of increased nucleotide degradation. Furthermore, this characteristic decrease of AdNs suggests that increased nucleotide degradation contributes to the general pathophysiology of skeletal muscle atrophy. In view of the numerous energetic, and non-energetic, roles of AdNs in skeletal muscle, investigations into the physiological consequences of AdN degradation may provide valuable insight into the mechanisms of muscle atrophy.

HPLC method for measurement of purine nucleotide degradation products in cerebrospinal fluid

1996 ◽  
Vol 42 (5) ◽  
pp. 756-760 ◽  
Author(s):  
L Kuracka ◽  
T Kalnovicová ◽  
B Líska ◽  
P Turcáni
Keyword(s):  
Cerebrospinal Fluid ◽  
Uric Acid ◽  
Neurological Disorders ◽  
Limit Of Detection ◽  
Degradation Products ◽  
Potassium Phosphate ◽  
Hplc Method ◽  
Potassium Phosphate Buffer ◽  
Nucleotide Degradation

Abstract We describe a convenient method for the separation and quantification of xanthine, hypoxanthine, and uric acid in 20 microL of cerebrospinal fluid (CSF) with use of HPLC and ultraviolet detection. The analysis is performed on a Sepharon SGX C18 column and the elution system consists of potassium phosphate buffer, pH 5.1, with 20 mL/L methanol. The lower limit of detection was 4 pmol for hypoxanthine and xanthine and 6 pmol for uric acid. Analytical recoveries of purine metabolites ranged from 98.6% to 102.9%. The intra- and interassay CVs were <3%. The applicability of the method is illustrated with the determination of micromolar concentrations of xanthine, hypoxanthine, and uric acid in CSF samples obtained from 113 patients with various neurological disorders.

Influences of weight and thickness on cooking time required for various mechanically tenderized beef steaks to reach minimum safe internal temperature without resting

LWT ◽  
2019 ◽  
Vol 110 ◽  
pp. 365-369 ◽  
Author(s):  
Joyjit Saha ◽  
Divya Jaroni ◽  
Jacob Nelson ◽  
Chuck Willoughby ◽  
Conner McDaniel ◽  
...  
Keyword(s):  
Cooking Time ◽  
Internal Temperature ◽  
Beef Steaks ◽  
Time Required

scholarly journals Biochemical Response to Freezing in the Siberian Salamander Salamandrella keyserlingii

Biology ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1172
Author(s):  
Sergei V. Shekhovtsov ◽  
Nina A. Bulakhova ◽  
Yuri P. Tsentalovich ◽  
Ekaterina A. Zelentsova ◽  
Ekaterina N. Meshcheryakova ◽  
...  
Keyword(s):  
Degradation Products ◽  
Ice Formation ◽  
Low Molecular Weight ◽  
Biochemical Basis ◽  
Hindlimb Muscle ◽  
Adenosine Phosphate ◽  
Nucleotide Degradation ◽  
Quantitative Changes ◽  
Siberian Salamander

The Siberian salamander Salamandrella keyserlingii Dybowski, 1870 is a unique amphibian that is capable to survive long-term freezing at −55 °C. Nothing is known on the biochemical basis of this remarkable freezing tolerance, except for the fact that it uses glycerol as a low molecular weight cryoprotectant. We used 1H-NMR analysis to study quantitative changes of multiple metabolites in liver and hindlimb muscle of S. keyserlingii in response to freezing. For the majority of molecules we observed significant changes in concentrations. Glycerol content in frozen organs was as high as 2% w/w, which confirms its role as a cryoprotectant. No other putative cryoprotectants were detected. Freezing resulted in ischemia manifested as increased concentrations of glycolysis products: lactate and alanine. Unexpectedly, we detected no increase in concentrations of succinate, which accumulates under ischemia in various tetrapods. Freezing proved to be a dramatic stress with reduced adenosine phosphate pool and high levels of nucleotide degradation products (hypoxanthine, β-alanine, and β-aminoisobutyrate). There was also significant increase in the concentrations of choline and glycerophosphocholine, which may be interpreted as the degradation of biomembranes. Thus, we found that freezing results not only in macroscopical damage due to ice formation, but also to degradation of DNA and biomembranes.

Nucleotide Degradation Products in Cerebrospinal Fluid (CSF) in Inherited and Acquired Pathologies

2004 ◽  
Vol 23 (8-9) ◽  
pp. 1185-1187 ◽  
Author(s):  
L. D. Fairbanks ◽  
J. C. Harris ◽  
J. A. Duley ◽  
H. A. Simmonds
Keyword(s):  
Cerebrospinal Fluid ◽  
Degradation Products ◽  
Nucleotide Degradation

Adenine nucleotide degradation in the rabbit heart

1964 ◽  
Vol 207 (5) ◽  
pp. 1139-1145 ◽  
Author(s):  
Harold G. Richman ◽  
Leigh Wyborny
Keyword(s):  
Oxidative Phosphorylation ◽  
Metabolic Control ◽  
Adenine Nucleotide ◽  
Degradation Products ◽  
Total Content ◽  
Rabbit Heart ◽  
Isolated Rabbit Heart ◽  
Nucleotide Degradation ◽  
Principal Pathway ◽  
Intact Heart

Adenine nucleotide analysis of tissue and perfusates of the isolated rabbit heart were undertaken following hypoxia and uncoupled oxidative phosphorylation. During uncoupled oxidative phosphorylation, nucleotide degradation, primarily that of ATP, was three times as great as that observed during hypoxia. Although inosine and hypoxanthine were generally observed degradation products, adenosine was recovered only following uncoupled oxidative phosphorylation. Perfusion with 8-azaguanine, however, resulted in recovery of adenosine during both hypoxia and uncoupled oxidative phosphorylation. Washout studies demonstrated the rapid extracellular movement of adenosine and the total content of adenosine was uniformly greater in perfusates than in tissue. In no case was adenine nucleotide efflux observed nor phosphatase or deaminase activity in the perfusate demonstrated. In myocardium initial dephosphorylation to adenosine would appear to be the principal pathway of AMP degradation. The rapid extracellular movement of adenosine would justify its consideration as a mediator of metabolic control in the intact heart.

Adenine nucleotide degradation in slow-twitch red muscle

1990 ◽  
Vol 258 (2) ◽  
pp. C258-C265 ◽  
Author(s):  
P. C. Tullson ◽  
D. M. Whitlock ◽  
R. L. Terjung
Keyword(s):  
Soleus Muscle ◽  
High Performance ◽  
Adenine Nucleotide ◽  
Degradation Products ◽  
Adenine Nucleotides ◽  
Extended Period ◽  
Red Muscle ◽  
Slow Twitch ◽  
Nucleotide Degradation ◽  
Purine Degradation

The catabolism of adenine nucleotides (AdN) in rat soleus muscle (predominantly slow twitch) is very different from that in fast-twitch muscle. AMP deaminase is highly inhibited during brief (3 min) intense (120 tetani/min) in situ stimulation, resulting in little inosine 5'-monophosphate (IMP) accumulation (0.21 mumol/g). Even with ligation of the femoral artery during the same brief intense contraction conditions there is surprisingly little increase in IMP (0.37 mumol/g), although AdN depletion is evident (-1.30 mumol/g). We have tested the hypothesis that accumulation of purine nucleosides and bases accounts for the AdN depletion by measuring purine degradation products using high-performance liquid chromatography. There was no stoichiometric accumulation of purine degradation products to account for the observed AdN depletion even though metabolite recovery was essentially quantitative. We hypothesis that under these conditions AdN are converted to a form different from purine nucleoside and base degradation products. In contrast to the inhibition of AMP deamination seen during brief ischemia, slow-twitch muscle depletes a substantial fraction (28%) of muscle AdN (1.75 mumol/g) that can be accounted for stoichiometrically as purine degradation products during an extended 10-min ischemic period of mild (12 tetani/min) contraction conditions. IMP accumulation (1 mumol/g) is most prominent with inosine, accounting for 23% (0.4 mumol/g) of the depleted AdN, showing that slow-twitch red muscle is capable of both AMP deamination and the subsequent production of purine nucleosides during an extended period of ischemic contractions. The present results indicate that AdN metabolism in the soleus muscle is complex, yielding expected degradation products or a loss of total purines, depending on contraction conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

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