Vol.
188,
No.
October
15,
BIOCHEMICAL
1, 1992
AND
BIOPHYSICAL
RESEARCH
COMMUNICATIONS
Pages
1992
114-119
MOUSEBEPATIC MICllOSOMAL OXIDATIONOF ALIPBATIC ALDEBYDES(C, to &I) ‘I-UCARBOXYLICACIDS Kazuhito Watanabe il Tamihide Matsunaga a , Shizuo Naripatsu Ikuo Y&to 1 * * and Hidetoshi Yoshimura c
l
Department of Hygienic Chemistry, Faculty of Pharmaceutical llokuriku University, Kanazawa 920-11, Japan
’ *b ,
Sciences,
c Department of Food and Nutrition, Nakamura Gakuen College, Fukuoka 814-01, Japan Received
August
17,
1992
SUMlABY:Addition of saturated and a, fi-unsaturated aliphatic aldehydes (CI to CI1) significantly increased NAM oxidation with mouse hepatic microsoRs, and the aldehydes themselves were oxidized to the corresponding carboxylic acids. when these aldehyde substrates were incubated similarly under oxygen-18 gas and the carboxylic acids formed were analyzed by CC-i& after methylation, it was indicated that oxygen-18 was significantly incorporated into the carboxylic acids foned from (z, B-unsaturated aldehydes, but not significantly into the carboxylic acids formed from saturated aldehydes. These results indicate that enzyme and/or mechanism responsible for the oxidation of these two types of aldehydes is different from each other. 0 1992Academic Press,Inc.
Saturated and the lipid
a,
B-unsaturated
peroxidation
metabolized
(7,8).
or aldehyde dehydrogenase (3,9),
Our previous
fraction, studies
on the biological
It is well known that
to nontoxic alcohols
the nitochondrial
or carboxylic
sople of these
system (4-6), these toxic
and exert
aldehydes are
acids by alcohol dehydrogenase
which is mainly localized
in the cytosolic
or
respectively. demonstrated
oxygenase (MALDO),which is a particular oxidation
aldehydes have been regarded as
products of q icrosomal membranes (l-3).
aldehydes have the adverse effects mutagenic activity
aliphatic
that
hepatic
aldehyde
form of cytochrome P450, catalyzes the
of various aldehydes to the corresponding
* To whom all correspondence should be addressed. b Present address: Department of Biopharmaceutics, Sciences, Chiba University, Chiba 260, Japan. 0006-291X/92 $4.00 Copyright 0 1992 by Academic Press, Inc. All rights of reproduction in any form reserved.
microsomal
114
carboxylic
acids (10-12).
Faculty of Pharmaceutical
Vol.
188,
No.
liepatic
1, 1992
BIOCHEMICAL
microsomal
dehydrogenases,
saturated
and
length of eight
fractions
also
which are reported
products of lipid The present
AND
peroxidation
contain
RESEARCH
COMMUNICATIONS
membrane bound
to catalyze
the oxidation
aldehyde
of aldehydic
(13).
communication a,
BIOPHYSICAL
describes
B-unsaturated
hepatic
aliphatic
microsomal
oxidation
of
aldehydes having medium chain
to eleven carbons.
MAIERIALs AND METHDIE 1-iktanal, 1-nonanal, 1-decanal and 1-undecanal were purchased from Wako Pure C&m. Ind., Ltd.; Z-octenal and 2-nonenal were from Aldrich C&II. Co. Inc.; 2-decenal and 2-undecenal were from Tokyo Kasei Kogyo Co., Ltd.; NADPand glucose-tphosphate were from Doehringer Mannheim Cmbli.; glucose-6-phosphate dehydmgenase (type V) was from Sigma Chem. Co. and oxygen-18 gas (97 at&) was from Amersham International plc. Other chemicals used were of analytical reagent grade. Hepatic microsomes from male ddN mice (30 to 35 g) were prepared by the different centrifugation force described previously (14). Microsomal NADPHoxidation was assayed by the previous method (15). A typical incubation mixture for the microsomal oxidation of aldehyde substrates consisted of washed q icrosomes (0.4 g liver equivalent), 0.5 dl NADP, 10 mM glucose-6-phosphate, 10 ti MgCl2, 1.2 units glucose-6-phosphate dehydrogenase, 1 ag aldehyde substrate and 100 ti sodium-potassium phosphate buffer (pll 7.4) to make a final volume of 1 ml. The mixture was incubated at 37 “c for 30 q in under oxygen-18 gas, and the carboxylic acid metabolites formed were analyzed by CC-i@ as described previously (11). CC-K was performed with a JEDL CCC-06 gas chromatograph coupled with a JKDL JM5-DX-300 mass spectrometer and a JEOL JMADA 5000 muss data system. ‘lhe conditions were as follows: coltam, 2% OV-17 on Qlrumosorb W (SO-SOmesh, 3 napx 2 m); calm temperature 120 “c for l-o&anal, 2-octenal, 1-nonanal and 2-nonenal as substrates or 130 T for 1-decanal, 2decenal, I-undecanal and 2-undecenal as substrates; carrier gas, He 40 ql/rein; ionization energy, 70 eV; ionizing current, 300 PA. Under these conditions, the retention times of methyl ester of the carboxylic acids were 1.9 q in (loctanal), 2.9 q in (2-octenal), 3.2 min (1-nonana l), 3.4 q in (1-decanal), 4.7 min (2-nonenal), 5.1 min (2-decenal), 5.8 q in (1-undecanal) and 8.7 q in (2undecenal).
KESUL’ISAND DI5CUSION Ail aldehyde substrates NADPHoxidation NAlFll oxidation
except for 1-undecanal
with hepatic
q icrosomes (Table I).
by these aldehydes may be partially
NADPH-dependent electron
transport
system involving
these aidehydes could be metabolized.
reductase
NADPHoxidation
stimulated
The enhancement of the
due to their effects
contain
for metabolism of carbonyl compounds,
(16), which may also contribute
by the aldehyde substrates. 115
on the
cytochrome P450 by which
Hepatic microsomal fractions
other NADPH-dependent enzyme responsible carbonyl
significantly
to the stimulation
of the
vol.
BIOCHEMICAL
No. 1, 1992
188,
AND BIOPHYSICAL
RESEARCH COMMUNICATIONS
Table I. Effects of Allphatic Aldehydesou NAiMiOxidation in Mouse iiepatic Microsomes a , B-Unsaturated akiehydes
Saturated akiehydes NADPH oxidation x of coutrol (RolhiuM
Additions Control l-octaual 1-Nauanal 1-l)ecanal I-Uudecaual
9.7 14.7 12.5 11.5 10.3
f k + & f
Additions
100 0.7 b1 152 0.2 b1 129 0.1 b, 119 0.3 106
0.3
NADPiioxidation x of anltr01 (rpol/miu/n&
2-octeua1
14.0 14.3 a-Deceual 12.7 a-Undecenal 11.8
& f f +-
2-Nonenal
0.1 0.1 0.2 0.4
b, b, b1 l )
144 147 131 122
Values represent the meau + SE. of three experiments. Aldehydesadded to the incubation mixture were 4 4. a> Significantly different frets control (p< 0.05). b, Sigificautly different from coutrol (p< 0.01).
Our previous
studies
demonstrated
aromatic aldehydes (9-anthraldehyde, a , ~-unsaturated aliphatic
alicyclic
that MALDOcatalyzed
reported
of
cuminaldehyde and veratrum aidehyde),
aldehydes (myrtenal and peri llaldehyde)
aldehyde having aromatic ring
and Werringloer
the oxidation
and an
(3phenylpropionaldehyde)(ll).
NADPH-dependent
metabolism
Gans
of acetaldehyde,
propionaldehyde
and butyraldehyde
Terelius
reported that rat cytochrane P450 IIEl metabolized acetaldehyde
(18).
et al.
‘lhese findlngs
by rat hepatic microscnaes (1‘7).
suggest that aliphatic
Recently,
aldehydes may be aumuon substrates
for MALlHI. MALDDwhich catalyzes confirmed
by measuring
carboxyl ic acids.
oxidation
of aldehydes to carboxylic
the incorporation
of molecular
formed from l-o&anal
by mouse hepatic microsomes under oxygen-18 gas. at m/z 158 was apparently
acid formed from I-octanal,
and Z-octenal
Only a single molecular ion
whereas double molecular ions at m/z 156
that molecular oxygen was incorporated
from 2-octenal.
the
observed on the mass spectrum of methyl ester of the
and m/z 158 were shoun for that from 2-octenal. indicated
oxygen into
Figure 1 shows the mass chromatograms and mass spectra of
methyl esters of carboxylic acid metabolites
carboxylic
acids could be
The relative
The molecular ion at m/z 158 into 2-octenoic
abundance of the molecular
m/z 160 uas 100 : 13 for the metabolite
from 1-o&anal, 116
acid formed
ions at m/z 158 and
dnd that at m/z 156 and
Vol.
188,
No.
1, 1992
BIOCHEMICAL
IL xl
loo
150
MO
250
AND
BIOPHYSICAL
*1.5 361912 300
xl
RESEARCH
100
COMMUNICATIONS
150
xl0
6.2697
250
300
Fig. 1. Mass Chromtograas and Mass Spectra of Methylated Carboxylic Acid Metabolites Derived from l-O&anal and %-Octmal by Mouse Hepatic Microsomes under Oxygen-18 Gas.
r4/2 158 was 88 : 100 for the metabolite that 2-octenal is biotransformed
similar
q icrosomes.
The result
indicates
to the carboxylic acid by MAUI0 to some extent,
whereas other enzymes may contribute the hepatic
from 2-octenal.
to the biotransformation
Other aldehyde substrates
of 1-octanal
in
were also examined in a
manner and found to be metabolized to the corresponding carboxylic
acid
metabol i tes. The relative
abundance of molecular
oxygen-18 gas is smrized oxygen was significantly derived from the
a,
in Table II. incorporated
j3-unsaturated
acids derived from the saturated
although
the possibility
other could not entirely
indicate
formed under that molecular
acid metabolites
aldehydes, but not significantly
into the
aldehydes.
to the corresponding
enzy~s may contribute
The results
into the carboxylic
The present study suggests that the biotransformed
ions of carboxylates
a,
~-unsaturated
carboxylic
acids by MALllO, whereas other
to the microsomal oxidation that the reaction
of the saturated
mechanism may different
be ruled out at present. 117
aldehydes could be
MALllOcatalyzing
aldehydes, from each oxidation
vol.
188,
No.
BIOCHEMICAL
1, 1992
Table II.
AND
BIOPHYSICAL
RESEARCH
COMMUNICATIONS
Isotope Ratios in Molecular Ions of Carboxylic Acid Metabolites Formed by Mouse Repatic Microsomes under Oxygen-18 Gas Saturated
Substrates
a,
aldehydes
fi-Unsaturated
Substrates
Relative abundance ofM+Ions
aklehydes
Relative aimdance of M’ Ions
l-octanal (m/z 158:160)
100 : 13
2-octenal (m/z 156: 158)
88
: 100
1-Nonanal
100 : 37
2-Nonenal
77
: 100
63
: 100
(m/z 172:174)
(m/z 170:172)
I-rkcaoill
100 : 5
24ecenal
(m/z 186:188)
(Is/z 184:186)
1-Undecanal (m/z 200:202)
of aliphatic significance
100 : 4
aldehydes of lipid
98 : 100
a-Undml
(in/z 198:200)
is important
peroxidation
for understanding
in the microsoml
the toxicological
me&raw%
ACKNOWLEDGMENTS We thank Miss A. Nakashima of Analytical Center of llokuriku University for carrying out Cc-m analyses. lhis research was supported in part by a Grant-inAid from Scientific Research provided by the Ministry of Education, Science and Culture of Japan.
1. Benedetti, A., Ckqorti, M. and Esterbauer, H. (1980) Biochim. Biophys. Acta, 620, 281-296. 2. Poli, G., Dianzani, M.U., Cheeseman, K.H., Slater, T.F., Lang, J. and Estberbauer, ll. (1985) Biochem. J., 227, 629-638. 3. Esterbauer, Ii., Zollner, il. and Lang, J. (1985) Biochem. J., 228, 363-373. 4. Ferrali, M., Fulceri, R., Benedetti, A. and Coqorti, M. (1960) Res. a. Chea. Path. Phanwcol., 30, 99-112. 5. Paradisi, L., Panagini, C., Parola, M., Barnera, G. and Dianzani, M.U. (1985) Chem. Biol. Interact., 53, 209-21‘7. 6. Hauptlorenz, S., ESterbauer, H., Mall, W., Puqei, R., Schauenstein, E. and Pwchea&rf, B. (1985) Bio&em. Pharmacol., 34, 3803-3809. 7. Sasaki, Y. and Endo, R. (1978) Mutation Res., 54, 251-252. M.C., Levin, D.E., Esterbauer, ll. a. Marnett, L.J., Hurd, H.K., Hollstein, and Ames, B.N. (1985) Mutation Res., 148, 25-34. 9. Mitchell, D.Y. and Petersen, D.R. (1987) Toxic01 . Appl . Phareacol . , 87, 403-410. 10. Yawmoto, I., Watanabe, K., Narinmtsu, S. and Yoshinura, H. (1988) Biodwm. Biophys. Res. Cormun., 153, 779-782. 11. Watanabe, K. , Narimatsu, S., Yamamoto, I. and Yoshinura, H. (1990) Biochem. Biophys. Res. Corun., 166, 1308-1312. I. and YoshiaJra, H. (1991) 12. Watanabe, K., Narimtsu, S., Y-to, J. Biol. (%em., 266, 2709-2711. 13. Mitchell, D.Y. and Petersen, D.R. (1989) Arch. Biochem. Biophys., 269, 11-17. 118
Vol.
188, No. 1, 1992
BIOCHEMICAL
AND BIOPHYSICAL
RESEARCH COMMUNICATIONS
14. Watanabe, K., Ki ta, M., Yamamuto, I. and YoshiPura, Ii. (1983) J. Phanacobio-Dyn., 6, 581-587. 15. Watanabe, K., Y-to, I., Oguri, K. and Yoshimura, H. (1981) J. Pharmcobio-Dyn., 4, 604-611. 16. Sawada, il., Rara, A., Rayashibara, M., Nakayama, T., Usui, S. und Saeki, T. (1981) J. Biuchem., 90, 1077-1085. 17. Cans, G. and Werringloer, J. (1990) Procedings of the VIIIth International S-Gum on Microsaues and Drug Oxidations, p 126. 18. Terelius, Y., Norsten-Roog, C. ,Crddm, T. and Ingelman-Sundberg, M. (1991) Biochem. Biophys. Res. Gnmnm., 179, 689-694.
119
188,
No.
October
15,
BIOCHEMICAL
1, 1992
AND
BIOPHYSICAL
RESEARCH
COMMUNICATIONS
Pages
1992
114-119
MOUSEBEPATIC MICllOSOMAL OXIDATIONOF ALIPBATIC ALDEBYDES(C, to &I) ‘I-UCARBOXYLICACIDS Kazuhito Watanabe il Tamihide Matsunaga a , Shizuo Naripatsu Ikuo Y&to 1 * * and Hidetoshi Yoshimura c
l
Department of Hygienic Chemistry, Faculty of Pharmaceutical llokuriku University, Kanazawa 920-11, Japan
’ *b ,
Sciences,
c Department of Food and Nutrition, Nakamura Gakuen College, Fukuoka 814-01, Japan Received
August
17,
1992
SUMlABY:Addition of saturated and a, fi-unsaturated aliphatic aldehydes (CI to CI1) significantly increased NAM oxidation with mouse hepatic microsoRs, and the aldehydes themselves were oxidized to the corresponding carboxylic acids. when these aldehyde substrates were incubated similarly under oxygen-18 gas and the carboxylic acids formed were analyzed by CC-i& after methylation, it was indicated that oxygen-18 was significantly incorporated into the carboxylic acids foned from (z, B-unsaturated aldehydes, but not significantly into the carboxylic acids formed from saturated aldehydes. These results indicate that enzyme and/or mechanism responsible for the oxidation of these two types of aldehydes is different from each other. 0 1992Academic Press,Inc.
Saturated and the lipid
a,
B-unsaturated
peroxidation
metabolized
(7,8).
or aldehyde dehydrogenase (3,9),
Our previous
fraction, studies
on the biological
It is well known that
to nontoxic alcohols
the nitochondrial
or carboxylic
sople of these
system (4-6), these toxic
and exert
aldehydes are
acids by alcohol dehydrogenase
which is mainly localized
in the cytosolic
or
respectively. demonstrated
oxygenase (MALDO),which is a particular oxidation
aldehydes have been regarded as
products of q icrosomal membranes (l-3).
aldehydes have the adverse effects mutagenic activity
aliphatic
that
hepatic
aldehyde
form of cytochrome P450, catalyzes the
of various aldehydes to the corresponding
* To whom all correspondence should be addressed. b Present address: Department of Biopharmaceutics, Sciences, Chiba University, Chiba 260, Japan. 0006-291X/92 $4.00 Copyright 0 1992 by Academic Press, Inc. All rights of reproduction in any form reserved.
microsomal
114
carboxylic
acids (10-12).
Faculty of Pharmaceutical
Vol.
188,
No.
liepatic
1, 1992
BIOCHEMICAL
microsomal
dehydrogenases,
saturated
and
length of eight
fractions
also
which are reported
products of lipid The present
AND
peroxidation
contain
RESEARCH
COMMUNICATIONS
membrane bound
to catalyze
the oxidation
aldehyde
of aldehydic
(13).
communication a,
BIOPHYSICAL
describes
B-unsaturated
hepatic
aliphatic
microsomal
oxidation
of
aldehydes having medium chain
to eleven carbons.
MAIERIALs AND METHDIE 1-iktanal, 1-nonanal, 1-decanal and 1-undecanal were purchased from Wako Pure C&m. Ind., Ltd.; Z-octenal and 2-nonenal were from Aldrich C&II. Co. Inc.; 2-decenal and 2-undecenal were from Tokyo Kasei Kogyo Co., Ltd.; NADPand glucose-tphosphate were from Doehringer Mannheim Cmbli.; glucose-6-phosphate dehydmgenase (type V) was from Sigma Chem. Co. and oxygen-18 gas (97 at&) was from Amersham International plc. Other chemicals used were of analytical reagent grade. Hepatic microsomes from male ddN mice (30 to 35 g) were prepared by the different centrifugation force described previously (14). Microsomal NADPHoxidation was assayed by the previous method (15). A typical incubation mixture for the microsomal oxidation of aldehyde substrates consisted of washed q icrosomes (0.4 g liver equivalent), 0.5 dl NADP, 10 mM glucose-6-phosphate, 10 ti MgCl2, 1.2 units glucose-6-phosphate dehydrogenase, 1 ag aldehyde substrate and 100 ti sodium-potassium phosphate buffer (pll 7.4) to make a final volume of 1 ml. The mixture was incubated at 37 “c for 30 q in under oxygen-18 gas, and the carboxylic acid metabolites formed were analyzed by CC-i@ as described previously (11). CC-K was performed with a JEDL CCC-06 gas chromatograph coupled with a JKDL JM5-DX-300 mass spectrometer and a JEOL JMADA 5000 muss data system. ‘lhe conditions were as follows: coltam, 2% OV-17 on Qlrumosorb W (SO-SOmesh, 3 napx 2 m); calm temperature 120 “c for l-o&anal, 2-octenal, 1-nonanal and 2-nonenal as substrates or 130 T for 1-decanal, 2decenal, I-undecanal and 2-undecenal as substrates; carrier gas, He 40 ql/rein; ionization energy, 70 eV; ionizing current, 300 PA. Under these conditions, the retention times of methyl ester of the carboxylic acids were 1.9 q in (loctanal), 2.9 q in (2-octenal), 3.2 min (1-nonana l), 3.4 q in (1-decanal), 4.7 min (2-nonenal), 5.1 min (2-decenal), 5.8 q in (1-undecanal) and 8.7 q in (2undecenal).
KESUL’ISAND DI5CUSION Ail aldehyde substrates NADPHoxidation NAlFll oxidation
except for 1-undecanal
with hepatic
q icrosomes (Table I).
by these aldehydes may be partially
NADPH-dependent electron
transport
system involving
these aidehydes could be metabolized.
reductase
NADPHoxidation
stimulated
The enhancement of the
due to their effects
contain
for metabolism of carbonyl compounds,
(16), which may also contribute
by the aldehyde substrates. 115
on the
cytochrome P450 by which
Hepatic microsomal fractions
other NADPH-dependent enzyme responsible carbonyl
significantly
to the stimulation
of the
vol.
BIOCHEMICAL
No. 1, 1992
188,
AND BIOPHYSICAL
RESEARCH COMMUNICATIONS
Table I. Effects of Allphatic Aldehydesou NAiMiOxidation in Mouse iiepatic Microsomes a , B-Unsaturated akiehydes
Saturated akiehydes NADPH oxidation x of coutrol (RolhiuM
Additions Control l-octaual 1-Nauanal 1-l)ecanal I-Uudecaual
9.7 14.7 12.5 11.5 10.3
f k + & f
Additions
100 0.7 b1 152 0.2 b1 129 0.1 b, 119 0.3 106
0.3
NADPiioxidation x of anltr01 (rpol/miu/n&
2-octeua1
14.0 14.3 a-Deceual 12.7 a-Undecenal 11.8
& f f +-
2-Nonenal
0.1 0.1 0.2 0.4
b, b, b1 l )
144 147 131 122
Values represent the meau + SE. of three experiments. Aldehydesadded to the incubation mixture were 4 4. a> Significantly different frets control (p< 0.05). b, Sigificautly different from coutrol (p< 0.01).
Our previous
studies
demonstrated
aromatic aldehydes (9-anthraldehyde, a , ~-unsaturated aliphatic
alicyclic
that MALDOcatalyzed
reported
of
cuminaldehyde and veratrum aidehyde),
aldehydes (myrtenal and peri llaldehyde)
aldehyde having aromatic ring
and Werringloer
the oxidation
and an
(3phenylpropionaldehyde)(ll).
NADPH-dependent
metabolism
Gans
of acetaldehyde,
propionaldehyde
and butyraldehyde
Terelius
reported that rat cytochrane P450 IIEl metabolized acetaldehyde
(18).
et al.
‘lhese findlngs
by rat hepatic microscnaes (1‘7).
suggest that aliphatic
Recently,
aldehydes may be aumuon substrates
for MALlHI. MALDDwhich catalyzes confirmed
by measuring
carboxyl ic acids.
oxidation
of aldehydes to carboxylic
the incorporation
of molecular
formed from l-o&anal
by mouse hepatic microsomes under oxygen-18 gas. at m/z 158 was apparently
acid formed from I-octanal,
and Z-octenal
Only a single molecular ion
whereas double molecular ions at m/z 156
that molecular oxygen was incorporated
from 2-octenal.
the
observed on the mass spectrum of methyl ester of the
and m/z 158 were shoun for that from 2-octenal. indicated
oxygen into
Figure 1 shows the mass chromatograms and mass spectra of
methyl esters of carboxylic acid metabolites
carboxylic
acids could be
The relative
The molecular ion at m/z 158 into 2-octenoic
abundance of the molecular
m/z 160 uas 100 : 13 for the metabolite
from 1-o&anal, 116
acid formed
ions at m/z 158 and
dnd that at m/z 156 and
Vol.
188,
No.
1, 1992
BIOCHEMICAL
IL xl
loo
150
MO
250
AND
BIOPHYSICAL
*1.5 361912 300
xl
RESEARCH
100
COMMUNICATIONS
150
xl0
6.2697
250
300
Fig. 1. Mass Chromtograas and Mass Spectra of Methylated Carboxylic Acid Metabolites Derived from l-O&anal and %-Octmal by Mouse Hepatic Microsomes under Oxygen-18 Gas.
r4/2 158 was 88 : 100 for the metabolite that 2-octenal is biotransformed
similar
q icrosomes.
The result
indicates
to the carboxylic acid by MAUI0 to some extent,
whereas other enzymes may contribute the hepatic
from 2-octenal.
to the biotransformation
Other aldehyde substrates
of 1-octanal
in
were also examined in a
manner and found to be metabolized to the corresponding carboxylic
acid
metabol i tes. The relative
abundance of molecular
oxygen-18 gas is smrized oxygen was significantly derived from the
a,
in Table II. incorporated
j3-unsaturated
acids derived from the saturated
although
the possibility
other could not entirely
indicate
formed under that molecular
acid metabolites
aldehydes, but not significantly
into the
aldehydes.
to the corresponding
enzy~s may contribute
The results
into the carboxylic
The present study suggests that the biotransformed
ions of carboxylates
a,
~-unsaturated
carboxylic
acids by MALllO, whereas other
to the microsomal oxidation that the reaction
of the saturated
mechanism may different
be ruled out at present. 117
aldehydes could be
MALllOcatalyzing
aldehydes, from each oxidation
vol.
188,
No.
BIOCHEMICAL
1, 1992
Table II.
AND
BIOPHYSICAL
RESEARCH
COMMUNICATIONS
Isotope Ratios in Molecular Ions of Carboxylic Acid Metabolites Formed by Mouse Repatic Microsomes under Oxygen-18 Gas Saturated
Substrates
a,
aldehydes
fi-Unsaturated
Substrates
Relative abundance ofM+Ions
aklehydes
Relative aimdance of M’ Ions
l-octanal (m/z 158:160)
100 : 13
2-octenal (m/z 156: 158)
88
: 100
1-Nonanal
100 : 37
2-Nonenal
77
: 100
63
: 100
(m/z 172:174)
(m/z 170:172)
I-rkcaoill
100 : 5
24ecenal
(m/z 186:188)
(Is/z 184:186)
1-Undecanal (m/z 200:202)
of aliphatic significance
100 : 4
aldehydes of lipid
98 : 100
a-Undml
(in/z 198:200)
is important
peroxidation
for understanding
in the microsoml
the toxicological
me&raw%
ACKNOWLEDGMENTS We thank Miss A. Nakashima of Analytical Center of llokuriku University for carrying out Cc-m analyses. lhis research was supported in part by a Grant-inAid from Scientific Research provided by the Ministry of Education, Science and Culture of Japan.
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