Determination of Creatine, Creatinine, Arginine, Guanidinoacetic Acid, Guanidine, and Methyl-Guanidine in Biological Fluids

Pilsum, John F. Van; Martin, Robert P.; Kito, E.; Hess, Julie

doi:10.1016/s0021-9258(19)50788-8

Cited by 233 publications

(20 citation statements)

References 58 publications

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“…Urea was estimated by the method of Koritz and Cohen (9), with chloride added to intensify and standardize color values (1). Arginine was estimated colorimetrically by the method of Van Pilsum et al (18). Enzyme assays.…”

Section: Methodsmentioning

confidence: 99%

Control of arginine utilization in Neurospora

Weiss¹,

Davis²

1977

J Bacteriol

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The response of Neurospora to changes in the availibility of exogenous arginine was investigated. Upon addition of arginine to the growth medium, catabolism is initiated within minutes. This occurs prior to expansion of the arginine pool or augmentation of catabolic enzyme levels. (Basal levels are approximately 25% of those found during growth in arginine-supplemented medium.) Catabolism of arginine is independent of protein synthesis, indicating that the catabolic enzymes are active but that arginine is not available for catabolism unless present in the medium. Upon exhaustion of the supply of exogenous arginine, catabolism ceases abruptly, despite an expanded arginine pool and induced levels of the catabolic enzymes. The arginine pool supports protein synthesis until the cells regain their normal capacity for endogenous arginine synthesis. These observations, combined with the known small level of induction of arginine catabolic enzymes, non-repressibility of most biosynthetic enzymes, and vesicular localization of the bulk of the arginine pool, suggest that compartmentation plays a significant role in controlling arginine metabolism in Neurospora.

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Section: Methodsmentioning

confidence: 99%

Control of arginine utilization in Neurospora

Weiss¹,

Davis²

1977

J Bacteriol

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“…11A). It is well known from previous studies, that neurons in these brain areas are involved in the regulation of thermogenesis [47,83]. In the MnPO, we have not found statistical difference in the number of c-Fos-positive cells between genotypes; however, c-Fos expression was nearly three times higher (p<0.05) in the MPO of the Pacap -/-mice as compared to controls (Fig.…”

Section: Characteristics Of the Thermoregulatory Response In The Absence Of Pacapmentioning

confidence: 44%

“…9), which are the two principal autonomic cold-defense thermoeffectors [132]. The initial skin vasoconstriction seems to contradict the reported vasodilatory effect of PACAP38 [77,78], but this contradiction can be resolved by considering that in the current study PACAP38 was delivered into the lateral ventricle of the brain, from where it can broadly access the POA, where neurons of the thermoeffector pathway for tail skin vasomotor tone are situated [83,133]. Therefore, it is plausible that PACAP38 acted on central thermoregulatory elements resulting in skin vasoconstriction, but when the peptide spread to more distant (non-thermoregulatory) areas, it caused vasodilatory effect, which was also observed in our study ~40 min after PACAP38 injection (Fig.…”

Section: Discussionmentioning

confidence: 70%

“…Further studies are needed to assess whether the LPS-induced phosphorylation of cPLA2 is altered in the lungs of Tacr1 −/− mice in addition to the decreased COX-2 protein expression as shown in this study. A potential link in signal transduction between SP and COX-2 may coexist through PKC, as it was shown earlier that inhibitory effects of SP are mediated, at least in part by PKC isoenzymes (82), which play a key role in the biosynthesis of PGE2, likely by regulating the induction of COX-2 (83).…”

Section: Discussionmentioning

confidence: 94%

“…ALT and AST activities in serum were determined according to the method of Reitman and Frankel, 79 whereas GGT levels were assessed by the Szasz method. 80 Total plasma bilirubin level, BUN, and creatinine concentration was determined according to the method described by Jendrassik et al, 81 Patton and Crouch, 82 and Van Pilsum, 83 respectively.…”

Section: Biochemical Assaysmentioning

confidence: 99%

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Investigation of the receptorial and molecular mediators of systemic inflammation in different animal models

Pákai

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Systemic inflammation is accompanied by an increased production of reactive oxygen species (ROS) and by either fever or hypothermia (or both). To study aseptic systemic inflammation, it is often induced in rats by the intravenous administration of bacterial lipopolysaccharide (LPS). Knowing that bilirubin is a potent ROS scavenger, we compared responses to LPS between normobilirubinemic Gunn rats (heterozygous, asymptomatic; J/C) and hyperbilirubinemic Gunn rats (homozygous, jaundiced; J/J) to establish whether ROS mediate fever and hypothermia in aseptic systemic inflammation. These two genotypes correspond to undisturbed versus drastically suppressed (by bilirubin) tissue accumulation of ROS, respectively. A low dose of LPS (10 mg/kg) caused a typical triphasic fever in both genotypes, without any intergenotype differences. A high dose of LPS (1,000 mg/kg) caused a complex response consisting of early hypothermia followed by late fever. The hypothermic response was markedly exaggerated, whereas the subsequent fever response was strongly attenuated in J/J rats, as compared to J/C rats. J/J rats also tended to respond to 1,000 mg/ kg with blunted surges in plasma levels of all hepatic enzymes studied (alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase), thus suggesting an attenuation of hepatic damage. We propose that the reported exaggeration of LPS-induced hypothermia in J/J rats occurs via direct inhibition of nonshivering thermogenesis by bilirubin and possibly via a direct vasodilatatory action of bilirubin in the skin. This hypothermiaexaggerating effect might be responsible, at least in part, for the observed tendency of J/J rats to be protected from LPS-induced hepatic damage. The attenuation of the fever response to 1,000 mg/kg could be due to either direct actions of bilirubin on thermoeffectors or the ROS-scavenging action of bilirubin. However, the experiments with 10 mg/kg strongly suggest that ROS signaling is not involved in the fever response to low doses of LPS.

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