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Selenium and glutathione-enzymes levels in alcoholics
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Antioxidant Enzymes SELENIUM AND GLUTATHIONE-ENZYMES LEVELS IN ALCOHOLICS T. Westermarck, H. Mussalo-Rauhamaa, P. F. Atroshi, P. Ktirkkliinen, K. Pokolainen, J. Lehto, and U.-R. Nordberg. University of Helsinki; National Public Health Institute; College of Veterinary Medicine; Helsinki Central Institute, Kirkkonummi, SF02400 Finland Ethanol is a lipid solvent with marked effects on the cell membranes. One natural target for the actions of ethanol may be the membrane polyunsaturated fatty acids. Ethyl alcohol is a hydroxyl radical scavenger. Low levels of ethanol may stimulate and higher ones inhibit lipid peroxidation and prostaglandin formation. The peroxidation of arachidonic acid is controlled by specific peroxidases, GSH-S-transferases, antioxidants and specific cofactors. Twenty-one drunkenness subjects and 21 healthy volunters (mean age 35.5 years) were examinate after they had fasted for 24 hrs. Serum selenium level,was 121.0 It g/1 in healthy volunters, and 68.0 /ag/l in alcoholics (p<0.01). Erythrocyte glutathione peroxidase was substantially and significantly reduced in alcoholics. Serum gamma-GT level was increased by 35% compared to the values of the controls, although selenium deficiency may contribute to alcoholic liver injury, it is also possible that low serum Se levels may, in part, simply be a consequence of liver disorders. The generation of high levels of cellular free radicals during the metabolism of ethanol may exceed the capacity for antioxidant defence and contribute to the developement of ethanol-induced liver damage.
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PI~JEFERENTIAL EXPRESS I0 N O F SUPEI~OXIDE DIS MIYrASIE GE~'qEIN TIIE N E U R O MYmLANIN-PIGNiENTED NEITRONS O F T H E SUBST~NTIA NIGRA :EV[PLICATIONS F O R P ~ S O N ' S DISEASE.
Zha~ P.*,CebaUos"I(I'L HirschE.. LafonM'.. SinetP. M'(I'L A~'idY and F. INSEI~'viU 289, H6pkal de la Salp6~6re 75013 PARIS,(1) URA CNRS13357 Laboratolrc dc Bic~'h;,'~;¢Gdn~tiquc - H6pkal Necker Path FRANCE The dop*mlrtcrgicncuroas primarilyaffectedin Parklmon's dlseascarc the mcl~,i:'edneurons of the substantiaai~a pars compacta.The involvement of oxygen frecradicalshas bccn consideredas a potentialcytotoxiccause of ceLl death.This lead to search for specificcharacteristicsof toxicspecies dcfen.sc systemin thesenlgralneurons.Supero:ddc dismutase (SOD) which catalysesthe conversionof supcroxide radicalsto hydrogen peroxide was e'rnm;,~ed. The levelof CuZn dependent S O D (CuZ.nSOD) gcnc expressionwas studied at cellularlevel in human rnesencephalon post-mortcm, by in siru hybridization u~ng a 35-S-labelled e D N A probe komologous to human C,,7~OD mR.NA. Labelledcellswere dcmsclydistributedin the substandaaigra pars compacta,some cellswere present in the ventraltegmenral area.95 % of the positivelyhybridizedhigralcellswere the largene uromelan.in-cont~;ning ceils, indicating O, TnROD gone is preferentially expressed in the pigmented
dopamincrgicnearoas. The high levels of C'~7~SOD traascrlp~ suggest the biochemicalpathwaysleadingto toxicoxygenspedes formationare ac.t.iv'¢~thu.s requiring a high Ca~7~$OD protein to facilitate removalof the toxic radicals. Alternatively, a high C ~ O D acclivity might contr~ut* to the neu.rodegenerativeprocess itself. The nigralm¢ianlzcd neurons represent a subsetof dopaminergic.cells
with respect to their oxygen defease system. Th~ may account for their _pr_efeLendalvulnerabiliP/-m_P_ar kinson'.s_discase.
CHANGESOF SUPEROXIDEBISMUTASEIN CHINESEELDERLYAND
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MULTIPLE ORGAN SYSTEM FAILURE PATIENTS Ling Y., Ying-jie D., llao-shan J. and Ling Z.
Institute of Gerontology and #~riatric, Chinese Great Wa!l Hospital, Beijing 100853, P. R. China In order to study the relation between supero×ide dismutase (SOD) activity and senile, htminal chemiluminescence microde termination method was taken for SOD activity assay in red cell chloroform-ethanol extract of three group bloed dor.,ors. SOB activities of group B (aged 95-105,6 male and 22 female) and group C (aged 60-70, 30 male) were markedly lower than the control, group A (aged 45-5.% 13 male and 15 female)(p ( 0.01). Meanwhile, the red cell SOD activity of 18 rases of multiple organ failure in the elderly (~FE) was measured. SOD activity in NOFE decreased 52.87~ comparing with the group A (p < 0.01), decreased 2.q.63~ comparingwith the group C (p < I}.05) and decreased 25.,1,~ comparingwith the longlived. The results suggest that 300 activity reflect the pathologic senile of human bodies while the biological age. Although the longlived person was at the age ttp to 105, the SOD activity had no difference with group C. These old men were in good health and activity. It means that healthy people has less dameged hy free radicals, or higher SOl} activity. SOD activity is a good inde× for health.
R E A C T I O N OF HOCI W I T H S U P E R O X I D E DISMUTASE, CATALASE, G L U T A T H I O N E P E R O X I D A S E AND E B S E L E N O k e z i e I. A r u o m a and Barry H a l l i w e l l B i o c h e m i s t r y Department, U n i v e r s i t y of L o n d o n K i n g ' s College, Strand, L o n d o n W C 2 R 2LS, UK Excess p r o d u c t i o n of r e a c t i v e oxygen species has been implicated in the p a t h o l o g y of several human diseases. A c t i v a t e d n e u t r o p h i l s c o n t a i n the enzyme m y e ~ o p e r o x i d a s e , w h i c h uses H202 to oxidize CI ions into a p o w e r f u l oxidant that has been i d e n t i f i e d as HOCI. HOCI g e n e r a t e d at sites of i n f l a m m a t i o n can have m u l t i p l e effects. The p o s s i b i l i t y that a n t i o x i d a n t enzymes as well as e b s e l e n could s c a v e n g e HOCI in vivo at a b i o l o g ically s i g n i f i c a n t rate was e x a m i n e d by t e s t i n g their a b i l i t y to protect a l p h a - l - a n t i p r o t e i n a s e , a major p h y s i o l o g i c a l target of HOCI attack. G l u t a t h i o n e p e r o x i d a s e was rapidly i n a c t i v a t e d by HOCI. E b s e l e n w h i c h has been shown to exert g l u t a t h i o n e p e r o x i d a s e - l i k e a c t i v i t y with peroxide s u b s t r a t e s was r e s i s t a n t to o x i d a t i v e attack by HOCI. S u p e r o x i d e d i s m u t a s e p r o t e c t e d alphal - a n t i p r o t e i n a s e and was more r e s i s t e n t to HOCI c o m p a r e d with catalase. HOCI d a m a g e d the haem f u n c t i o n in c a t a l a s e hence r a i s i n g the p o s s i b i l ity that c a t a l a s e may not be a useful antii n f l a m m a t o r y agent since iron ions lost from the p r o t e i n may be p r o - i n f l a m m a t o r y .
14.40
14.37
Antioxidant Enzymes SELENIUM AND GLUTATHIONE-ENZYMES LEVELS IN ALCOHOLICS T. Westermarck, H. Mussalo-Rauhamaa, P. F. Atroshi, P. Ktirkkliinen, K. Pokolainen, J. Lehto, and U.-R. Nordberg. University of Helsinki; National Public Health Institute; College of Veterinary Medicine; Helsinki Central Institute, Kirkkonummi, SF02400 Finland Ethanol is a lipid solvent with marked effects on the cell membranes. One natural target for the actions of ethanol may be the membrane polyunsaturated fatty acids. Ethyl alcohol is a hydroxyl radical scavenger. Low levels of ethanol may stimulate and higher ones inhibit lipid peroxidation and prostaglandin formation. The peroxidation of arachidonic acid is controlled by specific peroxidases, GSH-S-transferases, antioxidants and specific cofactors. Twenty-one drunkenness subjects and 21 healthy volunters (mean age 35.5 years) were examinate after they had fasted for 24 hrs. Serum selenium level,was 121.0 It g/1 in healthy volunters, and 68.0 /ag/l in alcoholics (p<0.01). Erythrocyte glutathione peroxidase was substantially and significantly reduced in alcoholics. Serum gamma-GT level was increased by 35% compared to the values of the controls, although selenium deficiency may contribute to alcoholic liver injury, it is also possible that low serum Se levels may, in part, simply be a consequence of liver disorders. The generation of high levels of cellular free radicals during the metabolism of ethanol may exceed the capacity for antioxidant defence and contribute to the developement of ethanol-induced liver damage.
14.39
PI~JEFERENTIAL EXPRESS I0 N O F SUPEI~OXIDE DIS MIYrASIE GE~'qEIN TIIE N E U R O MYmLANIN-PIGNiENTED NEITRONS O F T H E SUBST~NTIA NIGRA :EV[PLICATIONS F O R P ~ S O N ' S DISEASE.
Zha~ P.*,CebaUos"I(I'L HirschE.. LafonM'.. SinetP. M'(I'L A~'idY and F. INSEI~'viU 289, H6pkal de la Salp6~6re 75013 PARIS,(1) URA CNRS13357 Laboratolrc dc Bic~'h;,'~;¢Gdn~tiquc - H6pkal Necker Path FRANCE The dop*mlrtcrgicncuroas primarilyaffectedin Parklmon's dlseascarc the mcl~,i:'edneurons of the substantiaai~a pars compacta.The involvement of oxygen frecradicalshas bccn consideredas a potentialcytotoxiccause of ceLl death.This lead to search for specificcharacteristicsof toxicspecies dcfen.sc systemin thesenlgralneurons.Supero:ddc dismutase (SOD) which catalysesthe conversionof supcroxide radicalsto hydrogen peroxide was e'rnm;,~ed. The levelof CuZn dependent S O D (CuZ.nSOD) gcnc expressionwas studied at cellularlevel in human rnesencephalon post-mortcm, by in siru hybridization u~ng a 35-S-labelled e D N A probe komologous to human C,,7~OD mR.NA. Labelledcellswere dcmsclydistributedin the substandaaigra pars compacta,some cellswere present in the ventraltegmenral area.95 % of the positivelyhybridizedhigralcellswere the largene uromelan.in-cont~;ning ceils, indicating O, TnROD gone is preferentially expressed in the pigmented
dopamincrgicnearoas. The high levels of C'~7~SOD traascrlp~ suggest the biochemicalpathwaysleadingto toxicoxygenspedes formationare ac.t.iv'¢~thu.s requiring a high Ca~7~$OD protein to facilitate removalof the toxic radicals. Alternatively, a high C ~ O D acclivity might contr~ut* to the neu.rodegenerativeprocess itself. The nigralm¢ianlzcd neurons represent a subsetof dopaminergic.cells
with respect to their oxygen defease system. Th~ may account for their _pr_efeLendalvulnerabiliP/-m_P_ar kinson'.s_discase.
CHANGESOF SUPEROXIDEBISMUTASEIN CHINESEELDERLYAND
14.38
MULTIPLE ORGAN SYSTEM FAILURE PATIENTS Ling Y., Ying-jie D., llao-shan J. and Ling Z.
Institute of Gerontology and #~riatric, Chinese Great Wa!l Hospital, Beijing 100853, P. R. China In order to study the relation between supero×ide dismutase (SOD) activity and senile, htminal chemiluminescence microde termination method was taken for SOD activity assay in red cell chloroform-ethanol extract of three group bloed dor.,ors. SOB activities of group B (aged 95-105,6 male and 22 female) and group C (aged 60-70, 30 male) were markedly lower than the control, group A (aged 45-5.% 13 male and 15 female)(p ( 0.01). Meanwhile, the red cell SOD activity of 18 rases of multiple organ failure in the elderly (~FE) was measured. SOD activity in NOFE decreased 52.87~ comparing with the group A (p < 0.01), decreased 2.q.63~ comparingwith the group C (p < I}.05) and decreased 25.,1,~ comparingwith the longlived. The results suggest that 300 activity reflect the pathologic senile of human bodies while the biological age. Although the longlived person was at the age ttp to 105, the SOD activity had no difference with group C. These old men were in good health and activity. It means that healthy people has less dameged hy free radicals, or higher SOl} activity. SOD activity is a good inde× for health.
R E A C T I O N OF HOCI W I T H S U P E R O X I D E DISMUTASE, CATALASE, G L U T A T H I O N E P E R O X I D A S E AND E B S E L E N O k e z i e I. A r u o m a and Barry H a l l i w e l l B i o c h e m i s t r y Department, U n i v e r s i t y of L o n d o n K i n g ' s College, Strand, L o n d o n W C 2 R 2LS, UK Excess p r o d u c t i o n of r e a c t i v e oxygen species has been implicated in the p a t h o l o g y of several human diseases. A c t i v a t e d n e u t r o p h i l s c o n t a i n the enzyme m y e ~ o p e r o x i d a s e , w h i c h uses H202 to oxidize CI ions into a p o w e r f u l oxidant that has been i d e n t i f i e d as HOCI. HOCI g e n e r a t e d at sites of i n f l a m m a t i o n can have m u l t i p l e effects. The p o s s i b i l i t y that a n t i o x i d a n t enzymes as well as e b s e l e n could s c a v e n g e HOCI in vivo at a b i o l o g ically s i g n i f i c a n t rate was e x a m i n e d by t e s t i n g their a b i l i t y to protect a l p h a - l - a n t i p r o t e i n a s e , a major p h y s i o l o g i c a l target of HOCI attack. G l u t a t h i o n e p e r o x i d a s e was rapidly i n a c t i v a t e d by HOCI. E b s e l e n w h i c h has been shown to exert g l u t a t h i o n e p e r o x i d a s e - l i k e a c t i v i t y with peroxide s u b s t r a t e s was r e s i s t a n t to o x i d a t i v e attack by HOCI. S u p e r o x i d e d i s m u t a s e p r o t e c t e d alphal - a n t i p r o t e i n a s e and was more r e s i s t e n t to HOCI c o m p a r e d with catalase. HOCI d a m a g e d the haem f u n c t i o n in c a t a l a s e hence r a i s i n g the p o s s i b i l ity that c a t a l a s e may not be a useful antii n f l a m m a t o r y agent since iron ions lost from the p r o t e i n may be p r o - i n f l a m m a t o r y .
14.40