Blood sulfur-amino acid concentration reflects an impairment of liver transsulfuration pathway in patients with acute abdominal inflammatory processes

Abstract

Whole-blood free amino acids were measured in a control group made up of eight healthy women fasted for 12 h and also in eight patients with acute pancreatitis, five patients with acute cholecystitis and seven patients with acute appendicitis. Blood was withdrawn immediately on admission to hospital and again 3 d later following a controlled peripheral parenteral nutrition diet; this is with the exception of the appendicitis group. l-Cystathionine and l-methionine concentrations were significantly higher in pancreatitis and appendicitis patients when compared with controls. In the pancreatitis and cholecystitis patients, l-serine concentration was also significantly higher when compared with controls. The l-homocysteine concentration was significantly higher only in the appendicitis group when compared with the control group. l-Cystine concentration was unchanged in all the patients studied when compared with control subjects. The l-methionine : l-cystine ratio was significantly higher and the l-glutamine : l-cystine ratio was significantly lower in all the patients when compared with controls. The blood S-amino acid pattern reflects an impairment in liver transsulfuration pathway during acute abdominal processes. This work supports the idea that the l-methionine : l-cystine and l-glutamine : l-cystine ratios can be taken as good markers to evaluate the S-amino acid metabolism and suggests the importance of using N-acetylcysteine as a required nutrient in these situations.

Comparative effects of acute-methionine loading on the plasma sulfur-amino acids in NAC-supplemented HIV+ patients and healthy controls

“…The TS sequence is completed by a reaction catalyzed by gamma-cystathionase, which is responsible for the cleavage of L-cystathionine to yield Cys, alpha-ketobutyrate and NH 4 + . Hence, TS is an essential pathway allowing the synthesis of Cys from Met therefore, Met: Cys ratio can be taken as marker to evaluate the S-amino acid metabolism involved in Cys generation from Met (Viñ et al 2001).…”

“…Regarding a possible higher HIV+-induced Cys catabolism, it is known that, in post-absorptive state, muscle releases Cys that is taken up by the liver. Therefore, the basal Cys level is regulated primarily by the balance of normal post-absorptive skeletal muscle protein catabolism and liver uptake (Viñ et al 2001). The decreased blood Gln/L-cyst(e) ine ratio has been proposed as a good marker of an impaired hepatic L-cyst(e)ine catabolism (Dröge and Holm 1997).…”

“…The present HIV+ data showing 29% higher Gln/Cys (at baseline and under MetLo) along with similar Glu/Gln to the controls would suggest a HIV+ condition of normal glutaminogenesis (Glu/Gln) in a fair controlled whole-body catabolism (higher Gln/Cys). Moreover, considering that Met/Lcyst(e)ine and Gln/L-cyst(e)ine ratios can be taken as good markers to evaluate the S-amino acid metabolism (Viñ et al 2001), we can assume to have had more metabolic problems with Cys than with Met and Gln.…”

“…It has been considered that a higher urinary-sulfate output by HIV+ patients could be due to the fact that muscle excretes Cys to spare protein nitrogen (forming Gln in the liver) and restrain the body-protein catabolism (Dröge and Holm 1997). By the muscle excreting Cys to the liver (Sbrana et al 2004) the organism restrains the whole body-protein catabolism because Cys catabolism generates an increased formation of sulfate and protons which down-regulates the rate of urea production (Viñ et al 2001) allowing Gln synthesis and, therefore, nitrogen conservation, while the generated sulfate is excreted by urine. Even asymptomatic HIV-positive persons reveal, on average, a massive daily loss of sulfur, and may explain the widely observed decrease in cyst(e)ine and GSH levels.…”