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P-13 BLOOD GLUTATHIONE (GSH) DURING INTRAVENOUS (TPN) AND ENTERAL CENT) FEEDING. Sutton G.L.J., Taylor D. and Jackson A.A. Department of Human Nutrition and Surgery Southampton University, Southampton, England Oxido-reductive recycling of the tripeptide glutathione, Gamma-glutamyl-cysteinyl -glycinc, plays a central role in cellular protection against oxidant stress. The level of GSH in liver and blood is sensitive to dietary intake. We measured GSH by Beutler's method in the blood of patients whilst fasted and again after at least 3 days TPN (lOMJ, 14C of N) and in patients after at least 2 days of ENT (lOMJ, 12G of N). In a group of patients the CSH level was followed as they moved from TPN to ENT. mean GSH State Z Change State n= mmol/gHb Normal - Fasted -189.P=NS Fasted 11 5.6 c 0.3 Fasted - TPN - 1% P=NS TPN 9 5.5 + 0.3 Fasted - ENT +lloY"P(O.05 ENT 9 6.2 + 0.4 TPN - ENT +112'x P<O.O2 There was a depressed level of CSH during fasting that was not improved during TPN. There was a significant improvement in CSH when ENT was introduced to either the fasted or TPN state. There is little preformed cysteine in most intravenous feeding solutions. Cysteine is formed efficiently when methioninc is given ora'llybut not when given intravenously. We suggest that the low GSH seen during TPN is due to limited formation of cysteine in the splanchnic bed. Given the important role played by GSH in maintaining the cellular defences agaist damage, these observations may go some way towards explaining the superior efficacy of ENT over TPN, especially in the sickest patients, in whom the requirement for CSH may be increased. P.14 t!ETHIONINE MET)! CYSTATHIONINE (KY-ALAI AND CYSTINE (CYSIURINARYLOSSES DURINGTOTAL PARENTERAL NUTRITION(TPNI5. Iapichino, 6.Ronetti, I). Radri:zanl, A.Scherini, R. fialacrida, 6. Ron:oni, S. Recalcati, 6. Daaia. Istituto di Rnestesia e Pianimazione - flilaao - ITRLlb. The eulphuramino acid IAR)metabolism was investigated in 43 depleted (I)) and 30 critically i!l injured (1) patientsreceiving TPN. A ainisurB, intakeof 5 ng day-* *as provided, nitrogenIntake was suppliedwith different AA solutions(Sol. 1,?,3,41, yeldinga daily !lET load higher than 15-24 ag kg -I, !ET plasaa level and urinary loss increased, both relatedlinearly to !iET intake (piB.081 D; p(B.01 I). The increase of RET load caused the appearance of KY-ALPItraces In plasra and the increase ?f ACY-RLCI urinaryloss, which were always higher than reference. This increase #as linearly related to HET intake (pi0,RBl D and II, being the slope significantly higher in D group ipi0.B01). Cystine (CYS)plasma levelswere lou or normal,mhlle its urinaryoutput was 2-1 times greaterthan the nor& and significantly relatedto HET Input (pi0,0Bl D; pCB,01 Il. In conclusion cystatlaninase activityseeas unabie to cope rith the KY-ALEIload affectedby HET input,this in turn affectsCYS low levels.CYS is also excretedin an abnormally high amount,despiteits low concentration, suggesting a tubularlass. ZNTRDLS DEPLETED INJURED __________ M Sol. / - : 1 2 3 / : ‘, 4 Acyala-u I 8.3tU.t : 0.9+0.1*1.9+0.2* 0.;+0.1 I 2.:+0.3* 1.3+e.2* :,1+0.2* cys-u I 0.9t0.1 I 2.5+0.3* 3.6+0.3* 2.2ta.2+ ! - ;0.4+7.:* Cyr-pl : 34.5fb.l : 29.3+5.t* 53.5+4.4t 5?.?+4.8* I 27.5+3.:* ?0.7+?.1* :.;t5,qt net-In I - / 73+u.i 1u1+0.1 15t0.1 / lb?+?.0 24+!.0 ??tt.B Plasra ipil and urine (ui values as urn01 1-l; input tini as ag kg-' da;"' * - Significance v5 nom. 61

Methionine (MET), cystathionine (ACY-ALA) and cystine (CYS) urinary losses during total parenteral nutrition (TPN)

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Page 1: Methionine (MET), cystathionine (ACY-ALA) and cystine (CYS) urinary losses during total parenteral nutrition (TPN)

P-13 BLOOD GLUTATHIONE (GSH) DURING INTRAVENOUS (TPN) AND ENTERAL CENT) FEEDING. Sutton G.L.J., Taylor D. and Jackson A.A. Department of Human Nutrition and Surgery Southampton University, Southampton, England

Oxido-reductive recycling of the tripeptide glutathione, Gamma-glutamyl-cysteinyl -glycinc, plays a central role in cellular protection against oxidant stress. The level of GSH in liver and blood is sensitive to dietary intake. We measured GSH by Beutler's method in the blood of patients whilst fasted and again after at least 3 days TPN (lOMJ, 14C of N) and in patients after at least 2 days of ENT (lOMJ, 12G of N). In a group of patients the CSH level was followed as they moved from TPN to ENT.

mean GSH State Z Change State n= mmol/gHb Normal - Fasted -189. P=NS

Fasted 11 5.6 c 0.3 Fasted - TPN - 1% P=NS TPN 9 5.5 + 0.3 Fasted - ENT +lloY" P(O.05 ENT 9 6.2 + 0.4 TPN - ENT +112'x P<O.O2

There was a depressed level of CSH during fasting that was not improved during TPN. There was a significant improvement in CSH when ENT was introduced to either the fasted or TPN state. There is little preformed cysteine in most intravenous feeding solutions. Cysteine is formed efficiently when methioninc is given ora'lly but not when given intravenously. We suggest that the low GSH seen during TPN is due to limited formation of cysteine in the splanchnic bed. Given the important role played by GSH in maintaining the cellular defences agaist damage, these observations may go some way towards explaining the superior efficacy of ENT over TPN, especially in the sickest patients, in whom the requirement for CSH may be increased.

P.14 t!ETHIONINE MET)! CYSTATHIONINE (KY-ALAI AND CYSTINE (CYSI URINARY LOSSES DURING TOTAL PARENTERAL

NUTRITION (TPNI 5. Iapichino, 6. Ronetti, I). Radri:zanl, A. Scherini, R. fialacrida, 6. Ron:oni, S. Recalcati, 6. Daaia. Istituto di Rnestesia e Pianimazione - flilaao - ITRLlb.

The eulphur amino acid IAR) metabolism was investigated in 43 depleted (I)) and 30 critically i!l

injured (1) patients receiving TPN. A ainisur B, intake of 5 ng day-* *as provided, nitrogen Intake

was supplied with different AA solutions (Sol. 1 ,?,3,41, yelding a daily !lET load higher than 15-24 ag

kg -I, !ET plasaa level and urinary loss increased, both related linearly to !iET intake (piB.081 D;

p(B.01 I). The increase of RET load caused the appearance of KY-ALPI traces In plasra and the increase ?f ACY-RLCI urinary loss, which were always higher than reference. This increase #as linearly related

to HET intake (pi0,RBl D and II, being the slope significantly higher in D group ipi0.B01). Cystine (CYS) plasma levels were lou or normal, mhlle its urinary output was 2-1 times greater than

the nor& and significantly related to HET Input (pi0,0Bl D; pCB,01 Il. In conclusion cystatlaninase activity seeas unabie to cope rith the KY-ALEI load affected by HET input, this in turn affects CYS low levels. CYS is also excreted in an abnormally high amount, despite its low concentration,

suggesting a tubular lass.

ZNTRDLS DEPLETED INJURED __________

M Sol. / - : 1 2 3 / : ‘, 4 Acyala-u I 8.3tU.t : 0.9+0.1* 1.9+0.2* 0.;+0.1 I 2.:+0.3* 1.3+e.2* :,1+0.2*

cys-u I 0.9t0.1 I 2.5+0.3* 3.6+0.3* 2.2ta.2+ ! - ;0.4+7.:*

Cyr-pl : 34.5fb.l : 29.3+5.t* 53.5+4.4t 5?.?+4.8* I 27.5+3.:* ?0.7+?.1* :.;t5,qt

net-In I - / 73+u.i 1u1+0.1 15t0.1 / lb?+?.0 24+!.0 ??tt.B

Plasra ipil and urine (ui values as urn01 1-l; input tini as ag kg-' da;"' * - Significance v5 nom.

61