#METABOLOMICS WORKBENCH michaelsa93_20170413_144440_mwtab.txt DATATRACK_ID:887 STUDY_ID:ST000594 ANALYSIS_ID:AN000910 PROJECT_ID:PR000433
VERSION             	1
CREATED_ON             	April 17, 2017, 3:56 pm
#PROJECT
PR:PROJECT_TITLE                 	PGD2 and other lipid mediator changes in mouse adipose associated with
PR:PROJECT_TITLE                 	administration of an oral inhibitor of H-PGDS (HQL-79)
PR:PROJECT_SUMMARY               	This is an additional experiment being added onto a previous mouse feeding study
PR:PROJECT_SUMMARY               	that aimed to identify changes in metabolites that occur in metabolic tissues in
PR:PROJECT_SUMMARY               	the obese state that are long-lasting and not reversed by weight loss. We
PR:PROJECT_SUMMARY               	observed in the previous mice feeding study that levels of PGD2 increased in HFD
PR:PROJECT_SUMMARY               	fed mice and stayed high after the diet switch. Other members of the
PR:PROJECT_SUMMARY               	Prostaglandin family followed a similar trend (15-deoxy PGJ2, PGJ2) and were
PR:PROJECT_SUMMARY               	specific to adipose tissue. Based on previously published data indicating that
PR:PROJECT_SUMMARY               	central injection of PGD2 stimulates food intake, we attempted to observe this
PR:PROJECT_SUMMARY               	effect using an oral PGD2 inhibitor of H-PGDS (HQL-79). In fact, the oral
PR:PROJECT_SUMMARY               	inhibitor of the H-PGDS (HQL-79) administered peripherally (oral gavage in mice
PR:PROJECT_SUMMARY               	at 30mg/kg dose) reduced daily food intake. Mice were divided into two groups
PR:PROJECT_SUMMARY               	termed Vehicle (Control) and HGL-79 (H-PGDS inhibitor). Each group was analyzed
PR:PROJECT_SUMMARY               	for lipid mediator changes (including PGD2) in adipose tissue by the Newman lab.
PR:PROJECT_SUMMARY               	Analytical results generally met quality control criterion with respect to
PR:PROJECT_SUMMARY               	surrogate recoveries and replicate precision. Surrogate recoveries were good for
PR:PROJECT_SUMMARY               	most oxylipins (58-76%), endocannabinoids (53-75%), and fatty acids (36%).
PR:PROJECT_SUMMARY               	Recovery precision was good for most analytes in these profiles, ranging from
PR:PROJECT_SUMMARY               	6-28% RSD for most surrogates. The precision for the LTB4 surrogate was higher
PR:PROJECT_SUMMARY               	than most others (38%). Analytical precision was assessed by duplicate analysis
PR:PROJECT_SUMMARY               	of two separate study samples. Analytical precision was 62 - 69% of analytes
PR:PROJECT_SUMMARY               	having <30% RSD for all profiles and correlation analysis for the analytes
PR:PROJECT_SUMMARY               	within these samples ranged from 0.90-0.99 R2. The complete data set is in the
PR:PROJECT_SUMMARY               	associated excel file (Osborn HQL-79 – Deliverable Data Newman Lab.xls). There
PR:PROJECT_SUMMARY               	were few statistically significant differences observed when comparing
PR:PROJECT_SUMMARY               	concentrations (pmol/gr) between the control and HGL-79 treatment groups.
PR:PROJECT_SUMMARY               	However, when we compared ratios we saw numerous differences between PGD2 and
PR:PROJECT_SUMMARY               	its metabolite d15-PGJ2 versus other prostaglandins. Specifically, ratios
PR:PROJECT_SUMMARY               	between PGD2 and other connected pathway metabolites indicate a shift toward
PR:PROJECT_SUMMARY               	PGE2 and PGF2a production instead of PGD2 (Figure 1) with HQL-79 treatment. The
PR:PROJECT_SUMMARY               	PGD2 and PGE2 metabolites ratio of d15-PGJ2/15-keto PGE2 was statistically
PR:PROJECT_SUMMARY               	significant (P<0.01) using a two-tailed t-test. The ratios of PGD2/PGE2 and
PR:PROJECT_SUMMARY               	PGD2/PGF2 had p values of P<0.09 and P=0.07), respectively. Considering that we
PR:PROJECT_SUMMARY               	were predicting changes that indicated less PGD2 production it may be
PR:PROJECT_SUMMARY               	justifiable to use one-tailed tests instead. In order to maintain consistency
PR:PROJECT_SUMMARY               	with the metabolomic data analysis in the previous study, I followed the same
PR:PROJECT_SUMMARY               	statistical protocol that Johannes preformed for the main Pilot study. Using R
PR:PROJECT_SUMMARY               	and Devium log transformed data. Since this was a two group comparision, if the
PR:PROJECT_SUMMARY               	data was normal a 2 tailed t-test was used and if not normal then Mann-Whitney
PR:PROJECT_SUMMARY               	was used. A far as the significance of a shift from PGD2 to PGE2 production, I
PR:PROJECT_SUMMARY               	found a nice review article that discusses in detail the role of prostaglandins
PR:PROJECT_SUMMARY               	in white adipose tissue (Flachs et al. 2013). In the review it cites articles
PR:PROJECT_SUMMARY               	that have shown PGE2 to induce UCP1, modulate lipolysis adipogenesis, and
PR:PROJECT_SUMMARY               	stimulate leptin release. On the other hand, PGD2 was shown to increase
PR:PROJECT_SUMMARY               	adipogenesis and weight gain. Its downstream product d15-PGJ2 has been shown to
PR:PROJECT_SUMMARY               	increase adipogenesis, adipocyte differentiation, and decrease leptin
PR:PROJECT_SUMMARY               	production. This is significant since I also observed that the ratio of d15-PGJ2
PR:PROJECT_SUMMARY               	to 15-keto PGE2 (the downstream product of PGE2) was also decreased. Another
PR:PROJECT_SUMMARY               	prostaglandin whose ratio versus PGD2 was different in the inhibitor group was
PR:PROJECT_SUMMARY               	PGF2a which has been shown to increase glucose transport in adipose tissue.
PR:INSTITUTE                     	University of California, San Diego
PR:DEPARTMENT                    	Department of Medicine
PR:LAST_NAME                     	Osborn
PR:FIRST_NAME                    	Olivia
PR:ADDRESS                       	9500 Gilman Dr., La Jolla, CA 92093
PR:EMAIL                         	oosborn@ucsd.edu
PR:PHONE                         	858-822-6645
PR:FUNDING_SOURCE                	NIH U24DK097154
#STUDY
ST:STUDY_TITLE                   	PGD2 and other lipid mediator changes in mouse adipose associated with
ST:STUDY_TITLE                   	administration of an oral inhibitor of H-PGDS (HQL-79)
ST:STUDY_SUMMARY                 	This is an additional experiment being added onto a previous mouse feeding study
ST:STUDY_SUMMARY                 	that aimed to identify changes in metabolites that occur in metabolic tissues in
ST:STUDY_SUMMARY                 	the obese state that are long-lasting and not reversed by weight loss. We
ST:STUDY_SUMMARY                 	observed in the previous mice feeding study that levels of PGD2 increased in HFD
ST:STUDY_SUMMARY                 	fed mice and stayed high after the diet switch. Other members of the
ST:STUDY_SUMMARY                 	Prostaglandin family followed a similar trend (15-deoxy PGJ2, PGJ2) and were
ST:STUDY_SUMMARY                 	specific to adipose tissue. Based on previously published data indicating that
ST:STUDY_SUMMARY                 	central injection of PGD2 stimulates food intake, we attempted to observe this
ST:STUDY_SUMMARY                 	effect using an oral PGD2 inhibitor of H-PGDS (HQL-79). In fact, the oral
ST:STUDY_SUMMARY                 	inhibitor of the H-PGDS (HQL-79) administered peripherally (oral gavage in mice
ST:STUDY_SUMMARY                 	at 30mg/kg dose) reduced daily food intake. Mice were divided into two groups
ST:STUDY_SUMMARY                 	termed Vehicle (Control) and HGL-79 (H-PGDS inhibitor). Each group was analyzed
ST:STUDY_SUMMARY                 	for lipid mediator changes (including PGD2) in adipose tissue by the Newman lab.
ST:STUDY_SUMMARY                 	Analytical results generally met quality control criterion with respect to
ST:STUDY_SUMMARY                 	surrogate recoveries and replicate precision. Surrogate recoveries were good for
ST:STUDY_SUMMARY                 	most oxylipins (58-76%), endocannabinoids (53-75%), and fatty acids (36%).
ST:STUDY_SUMMARY                 	Recovery precision was good for most analytes in these profiles, ranging from
ST:STUDY_SUMMARY                 	6-28% RSD for most surrogates. The precision for the LTB4 surrogate was higher
ST:STUDY_SUMMARY                 	than most others (38%). Analytical precision was assessed by duplicate analysis
ST:STUDY_SUMMARY                 	of two separate study samples. Analytical precision was 62 - 69% of analytes
ST:STUDY_SUMMARY                 	having <30% RSD for all profiles and correlation analysis for the analytes
ST:STUDY_SUMMARY                 	within these samples ranged from 0.90-0.99 R2. The complete data set is in the
ST:STUDY_SUMMARY                 	associated excel file (Osborn HQL-79 – Deliverable Data Newman Lab.xls). There
ST:STUDY_SUMMARY                 	were few statistically significant differences observed when comparing
ST:STUDY_SUMMARY                 	concentrations (pmol/gr) between the control and HGL-79 treatment groups.
ST:STUDY_SUMMARY                 	However, when we compared ratios we saw numerous differences between PGD2 and
ST:STUDY_SUMMARY                 	its metabolite d15-PGJ2 versus other prostaglandins. Specifically, ratios
ST:STUDY_SUMMARY                 	between PGD2 and other connected pathway metabolites indicate a shift toward
ST:STUDY_SUMMARY                 	PGE2 and PGF2a production instead of PGD2 (Figure 1) with HQL-79 treatment. The
ST:STUDY_SUMMARY                 	PGD2 and PGE2 metabolites ratio of d15-PGJ2/15-keto PGE2 was statistically
ST:STUDY_SUMMARY                 	significant (P<0.01) using a two-tailed t-test. The ratios of PGD2/PGE2 and
ST:STUDY_SUMMARY                 	PGD2/PGF2 had p values of P<0.09 and P=0.07), respectively. Considering that we
ST:STUDY_SUMMARY                 	were predicting changes that indicated less PGD2 production it may be
ST:STUDY_SUMMARY                 	justifiable to use one-tailed tests instead. In order to maintain consistency
ST:STUDY_SUMMARY                 	with the metabolomic data analysis in the previous study, I followed the same
ST:STUDY_SUMMARY                 	statistical protocol that Johannes preformed for the main Pilot study. Using R
ST:STUDY_SUMMARY                 	and Devium log transformed data. Since this was a two group comparision, if the
ST:STUDY_SUMMARY                 	data was normal a 2 tailed t-test was used and if not normal then Mann-Whitney
ST:STUDY_SUMMARY                 	was used. A far as the significance of a shift from PGD2 to PGE2 production, I
ST:STUDY_SUMMARY                 	found a nice review article that discusses in detail the role of prostaglandins
ST:STUDY_SUMMARY                 	in white adipose tissue (Flachs et al. 2013). In the review it cites articles
ST:STUDY_SUMMARY                 	that have shown PGE2 to induce UCP1, modulate lipolysis adipogenesis, and
ST:STUDY_SUMMARY                 	stimulate leptin release. On the other hand, PGD2 was shown to increase
ST:STUDY_SUMMARY                 	adipogenesis and weight gain. Its downstream product d15-PGJ2 has been shown to
ST:STUDY_SUMMARY                 	increase adipogenesis, adipocyte differentiation, and decrease leptin
ST:STUDY_SUMMARY                 	production. This is significant since I also observed that the ratio of d15-PGJ2
ST:STUDY_SUMMARY                 	to 15-keto PGE2 (the downstream product of PGE2) was also decreased. Another
ST:STUDY_SUMMARY                 	prostaglandin whose ratio versus PGD2 was different in the inhibitor group was
ST:STUDY_SUMMARY                 	PGF2a which has been shown to increase glucose transport in adipose tissue.
ST:INSTITUTE                     	U.S.D.A. Western Human Nutrition Research Center, University of California,
ST:INSTITUTE                     	Davis
ST:DEPARTMENT                    	Nutrition
ST:LAST_NAME                     	Newman
ST:FIRST_NAME                    	John
ST:ADDRESS                       	430 W. Health Sciences Dr., Davis, CA 95616
ST:EMAIL                         	john.newman@ars.usda.gov
ST:PHONE                         	+1-530-752-1009
#SUBJECT
SU:SUBJECT_TYPE                  	Animal
SU:SUBJECT_SPECIES               	Mus musculus
SU:TAXONOMY_ID                   	10090
#SUBJECT_SAMPLE_FACTORS:         	SUBJECT(optional)[tab]SAMPLE[tab]FACTORS(NAME:VALUE pairs separated by |)[tab]Additional sample data
SUBJECT_SAMPLE_FACTORS           	Osb V1	Veh_01	Treatment:Vehicle	Organ=Adipose Tissue; Species=Mus Musculus
SUBJECT_SAMPLE_FACTORS           	Osb V2	Veh_02	Treatment:Vehicle	Organ=Adipose Tissue; Species=Mus Musculus
SUBJECT_SAMPLE_FACTORS           	Osb V3 Rep Avg.	Veh_03	Treatment:Vehicle	Organ=Adipose Tissue; Species=Mus Musculus
SUBJECT_SAMPLE_FACTORS           	Osb V4	Veh_04	Treatment:Vehicle	Organ=Adipose Tissue; Species=Mus Musculus
SUBJECT_SAMPLE_FACTORS           	Osb V5	Veh_05	Treatment:Vehicle	Organ=Adipose Tissue; Species=Mus Musculus
SUBJECT_SAMPLE_FACTORS           	Osb V6	Veh_06	Treatment:Vehicle	Organ=Adipose Tissue; Species=Mus Musculus
SUBJECT_SAMPLE_FACTORS           	Osb V7	Veh_07	Treatment:Vehicle	Organ=Adipose Tissue; Species=Mus Musculus
SUBJECT_SAMPLE_FACTORS           	Osb V8	Veh_08	Treatment:Vehicle	Organ=Adipose Tissue; Species=Mus Musculus
SUBJECT_SAMPLE_FACTORS           	Osb H1	HQL_01	Treatment:HQL-79	Organ=Adipose Tissue; Species=Mus Musculus
SUBJECT_SAMPLE_FACTORS           	Osb H2	HQL_02	Treatment:HQL-79	Organ=Adipose Tissue; Species=Mus Musculus
SUBJECT_SAMPLE_FACTORS           	Osb H3	HQL_03	Treatment:HQL-79	Organ=Adipose Tissue; Species=Mus Musculus
SUBJECT_SAMPLE_FACTORS           	Osb H4	HQL_04	Treatment:HQL-79	Organ=Adipose Tissue; Species=Mus Musculus
SUBJECT_SAMPLE_FACTORS           	Osb H5	HQL_05	Treatment:HQL-79	Organ=Adipose Tissue; Species=Mus Musculus
SUBJECT_SAMPLE_FACTORS           	Osb H6	HQL_06	Treatment:HQL-79	Organ=Adipose Tissue; Species=Mus Musculus
SUBJECT_SAMPLE_FACTORS           	Osb H7	HQL_07	Treatment:HQL-79	Organ=Adipose Tissue; Species=Mus Musculus
SUBJECT_SAMPLE_FACTORS           	Osb H8 Rep Avg.	HQL_08	Treatment:HQL-79	Organ=Adipose Tissue; Species=Mus Musculus
#COLLECTION
CO:COLLECTION_SUMMARY            	Mice were sacrificed between 10am and noon (ad libitum fed) and adipose tissue
CO:COLLECTION_SUMMARY            	collected and snap frozen and stored at –80oC.
CO:SAMPLE_TYPE                   	Adipose Tissue
#TREATMENT
TR:TREATMENT_SUMMARY             	C57BL6 male mice were treated with HQL-79 (H-PDGS inhibitor)  or vehicle
TR:TREATMENT_SUMMARY             	(control) by oral gavage at  a dose of 30mg/kg for 5 days.
TR:TREATMENT_DOSE                	30mg/kg
TR:TREATMENT_DOSEDURATION        	5 days
#SAMPLEPREP
SP:SAMPLEPREP_SUMMARY            	Oxylipins, endocannabinoids, and fatty acids were isolated using a Waters Ostro
SP:SAMPLEPREP_SUMMARY            	Sample Preparation Plate (Milford, MA). Adipose samples were pulverized and
SP:SAMPLEPREP_SUMMARY            	aliquoted (~10-15mg) were added to 2mL polypropylene tubes and spiked with a 5
SP:SAMPLEPREP_SUMMARY            	µL anti-oxidant solution (0.2 mg/ml solution BHT/EDTA in 1:1 MeOH:water) and 10
SP:SAMPLEPREP_SUMMARY            	μL 1000nM analytical deuterated surrogates. A total of 50 µL of methanol was
SP:SAMPLEPREP_SUMMARY            	added and the tube was placed in a Geno/Grinder for 30 sec. An additional 550µL
SP:SAMPLEPREP_SUMMARY            	isopropanol w/ 10mM ammonium formate & 1% formic acid and 100 uL water was added
SP:SAMPLEPREP_SUMMARY            	and the tube was placed in a Geno/Grinder for 30 sec before being centrifuged at
SP:SAMPLEPREP_SUMMARY            	10,000g for 5 min at room temp. The supernate was then transferred into the
SP:SAMPLEPREP_SUMMARY            	plate wells and samples were eluted into glass inserts containing 10 μL 20%
SP:SAMPLEPREP_SUMMARY            	glycerol by applying a vacuum at 15 Hg for 10 min. Eluent was dried by speed
SP:SAMPLEPREP_SUMMARY            	vacuum for 35 min at the medium BP setting, before switching to an aqueous
SP:SAMPLEPREP_SUMMARY            	setting for an additional 35 min. Once dry, samples were re-constituted with the
SP:SAMPLEPREP_SUMMARY            	internal standard 1-cyclohexyl ureido, 3-dodecanoic acid (CUDA) and 1-Phenyl
SP:SAMPLEPREP_SUMMARY            	3-Hexadecanoic Acid Urea (PHAU) at 100 nM (50:50 MeOH:CAN), vortexed 1 min,
SP:SAMPLEPREP_SUMMARY            	transferred to a spin filter (0.1 µm, Millipore, Billerica, MA), centrifuged
SP:SAMPLEPREP_SUMMARY            	for 3 min at 6ºC at <4500g (rcf), before being transferred to 2 mL LC-MS amber
SP:SAMPLEPREP_SUMMARY            	vials. Extracts were stored at -20ºC until analysis by UPLC-MS/MS. The internal
SP:SAMPLEPREP_SUMMARY            	standard was used to quantify the recovery of surrogate standards.
SP:SAMPLEPREP_PROTOCOL_FILENAME  	HQL-79_Lipid_Mediator_Data_Report.docx
#CHROMATOGRAPHY
CH:CHROMATOGRAPHY_TYPE           	Reversed phase
CH:INSTRUMENT_NAME               	Waters Acquity
CH:COLUMN_NAME                   	Waters Acquity BEH C18 (150 x 2.1mm, 1.7um)
CH:FLOW_GRADIENT                 	See protocol/methods file
CH:FLOW_RATE                     	0.25
CH:COLUMN_TEMPERATURE            	60 °C
CH:SOLVENT_A                     	0.1% acetic acid
CH:SOLVENT_B                     	90% ACN / 10% IPA
CH:INTERNAL_STANDARD             	See protocol/methods file
CH:RETENTION_TIME                	See protocol/methods file
CH:SAMPLE_INJECTION              	5 uL
CH:ANALYTICAL_TIME               	16 min
CH:WEAK_WASH_SOLVENT_NAME        	20% methanol, 10% isopropanol
CH:WEAK_WASH_VOLUME              	600 µL
CH:STRONG_WASH_SOLVENT_NAME      	50:50 Acetonitrile:Methanol
CH:STRONG_WASH_VOLUME            	600 µL
CH:SAMPLE_LOOP_SIZE              	17 uL
#ANALYSIS
AN:ANALYSIS_TYPE                 	MS
#MS
MS:MS_COMMENTS                   	-
MS:INSTRUMENT_NAME               	ABI Sciex API 4000 QTrap
MS:INSTRUMENT_TYPE               	Triple quadrupole
MS:MS_TYPE                       	ESI
MS:ION_MODE                      	NEGATIVE
#MS_METABOLITE_DATA
MS_METABOLITE_DATA:UNITS         	Concentration pmol/g
MS_METABOLITE_DATA_START
Samples	Veh_01	Veh_02	Veh_03	Veh_04	Veh_05	Veh_06	Veh_07	Veh_08	HQL_01	HQL_02	HQL_03	HQL_04	HQL_05	HQL_06	HQL_07	HQL_08
Factors	Treatment:Vehicle	Treatment:Vehicle	Treatment:Vehicle	Treatment:Vehicle	Treatment:Vehicle	Treatment:Vehicle	Treatment:Vehicle	Treatment:Vehicle	Treatment:HQL-79	Treatment:HQL-79	Treatment:HQL-79	Treatment:HQL-79	Treatment:HQL-79	Treatment:HQL-79	Treatment:HQL-79	Treatment:HQL-79
6-keto PGF1a	0.213	2.6	1.891	0.89	1.15	4.95	9.59	3.83	1.14	9.97	1.66	2.01	1.35	3.69	1.57	1.86
TXB2	0.768	1.68	0.8525	0.627	1.13	3.03	4.1	3.61	1.92	5.34	1.81	1.16	1.36	1.93	1.91	3.825
PGE1	2.11	1.02	1.1615	3.76	0.841	1.97	4.4	1.17	0.763	8.92	1.01	1.92	1.27	6.18	0.959	1.46
PGE2	25	17.2	13.7	32.2	10	50.1	52.6	25.8	22.5	78.4	23	23.8	34	67.4	18	26
15-Keto PGE2	0.433	0.216	0.1074	0.17	0.081	0.352	0.838	0.665	0.707	2.1	0.6	0.489	1.53	2.51	0.105	0.1821
PGD2	72.7	75.7	84.3	153	102	253	163	324	92.6	351	101	55.2	126	268	65	95.45
15-deoxy PGJ2	3.46	2.35	2.105	3.68	3.07	5.41	7.48	10.5	3.98	11.8	3.52	1.63	3.51	10.3	2.12	2.81
PGF2a	6.14	7.32	4.275	5.25	4.51	9.57	8.56	11.1	3.75	22	6.1	5.88	8.6	18.6	7.64	7.68
11-HETE	51.8	54.8	56.7	47.6	58.4	117	189	181	64.9	154	70.2	18.7	68.2	81	37.9	75.9
Lipoxin A4	31.8	10	6.67	34.4	7.55	20.6	27.7	23.2	17.4	38.8	16.9	15.9	27	46.1	4.51	8.195
6-trans-LTB4	2.3	1.39	2.08	1.91	1.82	2.66	10.3	6.36	3.37	4.77	2.74	0.917	3.78	2.99	1.72	3.57
5_15-DiHETE	0.706	0.676	1.3545	1.9	1.76	2.27	4.32	0.698	1.56	1.46	0.587	0.606	2.82	1.01	1.05	2.47
8_15-DiHETE	6.61	3.75	4.29	4.96	4.82	5.63	21.4	12.3	4.9	7.06	5.12	2.9	6.9	3.8	2.38	3.965
9_12_13-TriHOME	974	500	192.5	1350	165	695	620	775	573	1570	743	1380	1040	3570	112	207
9_10-e-DiHO	1480	631	255	1520	151	979	832	1070	613	2260	799	1370	943	3900	128	173.5
12_13-DiHOME	24.2	12.5	6.29	28.6	4.88	17.2	13.9	19	20.1	35.4	15.4	28.1	21.3	74.6	3.26	5.28
9_10-DiHOME	31.5	15.8	8.25	37	6.67	24.7	20.3	23.7	21.7	46	20.6	34.5	24	86.6	5.17	7.32
15_16-DiHODE	0.59	1.37	2.21		1.51	4.28	0.84	4.95	0.74	2.02	0.6	1.38		1.67	0.47	1.16
9_10-DiHODE	0.49	0.29	0.3	0.32	0.17	0.64	0.33	0.63	0.47	0.37	0.45	0.41	0.3	0.73	0.12	0.2
14_15-DiHETrE	0.923	0.595	0.5355	0.887	0.443	1.17	1.59	2.17	0.613	1.11	0.569	0.418	0.737	1.42	0.361	0.426
11_12-DiHETrE	1	0.426	0.342	0.709	0.394	0.979	1.07	1.13	0.473	1.02	0.457	0.251	0.547	0.987	0.209	0.3575
8_9-DiHETrE	0.846	0.716	0.382	1.21	0.273	1.04	1.18	0.84	0.356	0.913	0.304	0.375	0.602	0.911	0.739	0.4045
5_6-DiHETrE	0.362	0.233	0.1405	0.309	0.222	0.191	0.252	0.806	0.174	0.227	0.0808	0.12	0.357	0.233	0.0468	0.0904
17_18-DiHETE	31.1	30.7	23.2	39.4	30.1	34.3	39	39.9	29.9	47.6	30	21.7	54.6	22.5	29.4	19.3
19_20-DiHDoPA	1.59	1.46	1.995	1.25	1.42	2.87	4.26	7.77	0.929	2.26	0.994	0.732	0.605	1.63	0.88	1.915
13-HODE	1580	701	835.5	1430	934	1480	3790	2750	1110	2310	1460	847	1520	2370	406	1067
9-HODE	1370	560	583.5	1170	584	1130	1980	1950	997	1620	1130	727	1020	2070	328	700.5
13-HOTE	40.3	17.9	39.35	26.7	31.8	42.1	151	77.6	36.8	77.6	38.1	16.2	52.3	34	15.4	74.05
9-HOTE	2.3	1.25	1.81	1.53	0.931	1.66	1.51	5	3.63	3.02	1.15	0.714	1.46	3.57	1.19	2.41
20-HETE		0.712	1.415	1.68	1		2.82	4.68	7.46	0.434	0.1	1.23			1.36	
15-HETE	112	81.2	89.8	104	139	200	583	310	84.8	279	125	37.8	145	131	60.7	148
12-HETE	179	297	215.5	262	382	349	2020	928	163	960	273	172	413	270	172	348.5
9-HETE	52.5	46.7	57.5	37.1	50.9	84.4	137	153	71.6	88.6	70.5	9.91	64.9	53.3	29.6	65.3
8-HETE	42	32.8	33.8	33.1	40.7	57.4	128	108	45.9	80.8	49.5	9.29	50.9	44	22.9	47.1
5-HETE	71.8	43.2	37.75	51.4	49.9	82	135	151	54.4	117	61.7	16.7	67.1	82.3	22.3	50.25
15-HEPE	8.02	3.36	8.635	6.75	10.3	12.6	47.2	20	7.48	21.5	8.61	2.84	14.1	6.54	4.32	15.45
12-HEPE	7.24	15.9	11.14	10.3	13.2	19.1	40.7	41.9	7.52	43.8	11.7	8.27	14.2	15.9	7.02	18.25
9-HEPE	4.74	5.96	6.26	3.66	5.52	6.48	6.45	9.27	8.7	6.28	6.01	1.02	5.79	4.04	2.14	8.89
5-HEPE	6.67	4.05	3.63	4.24	3.25	7.18	7.65	10.1	3.13	7.1	5.21	1.84	7.09	4.75	1.73	4.95
17-HDoHE	29.3	17.9	37.4	33.2	46.7	45.4	280	115	49.1	116	55.2	22.3	66.8	45	36.1	87.25
14-HDoHE	98.7	38.6	116.05	90.9	110	125	1210	365	74.7	313	115	38	191	64.8	52.2	237.45
4-HDoHE	8.35	2.26	3.46	3.87	3.95	6.57	11	15.2	4.58	10.6	6.92	2.47	5.39	8.97	3.01	3.98
9_10-EpO	1570	345	135	721	63.3	417	580	982	451	1020	705	732	523	3420	72.7	113
12(13)-EpOME	49.2	17.8	30.3	27.9	12.7	29	32.9	63.2	59.7	50.9	36.6	30.1	36.1	101	19.2	32.5
9(10)-EpOME	61.3	19.6	34.35	34.5	14.2	30.5	37.1	67.8	65.3	66.3	41.1	38.7	41.7	127	20.3	32.8
12(13)-Ep-9-KODE	122	57	27.35	86.1	16.5	67.3	77.2	167	51.8	161	77.9	104	67.9	285	10.3	23.8
15(16)-EpODE	6.82	2.87	4.475	2.69	1.71	6.26	6.07	11.1	7.33	11.1	5.86	3.13	4.47	12.2	1.94	4.455
12(13)-EpODE	1.27	0.394	0.671	0.769	0.555	0.756	0.564	1.52	2.11	0.881	0.797	0.74	0.729	1.19	0.591	1.18
9(10)-EpODE	3.29	1.67	2.64	2.5	1.38	2.18	2.95	6.49	4.01	5.34	3.09	2.01	2.61	6.44	1.79	3.195
14(15)-EpETrE	6.76	4.62	6.765	5.26	3.52	5.38	5.64	11.6	14.9	8.79	4.07	3.63	5.75	10.7	5.8	6.965
11(12)-EpETrE	4.78	2.74	3.395	2.69	2.19	2.58	3.86	7.19	9.56	4.64	3.74	1.81	3.64	6.7	3.21	3.41
8(9)-EpETrE	4.78	2.3	3.555	2.95	2.19	3.01	3.48	9.32	10.1	5.53	4.1	2.44	3.77	6.6	2.84	3.01
19(20)-EpDPE	5.73	2.62	3.17	3.62	1.54	2.69	4.2	9.93	5.11	4.4	2.67	2.36	1.37	6.68	1.69	2.915
13-KODE	42.5	28.7	17.25	44.1	18	37.5	48.3	60.9	49.9	73.9	66.4	40.6	50.2	93	16.4	40.2
9-KODE	125	68.3	42.35	126	41.7	91.1	107	109	142	163	186	108	130	251	31.1	84.05
15-KETE	2.92	1.78	2.13	2.76	1.26	1.91	7.12	6.24	2.4	4.89	2.99	0.583	3.12	3.26	0.977	2.645
5-KETE	2.37	2.44	0.715	1.51	0.975	1.87	2.88	5.57	1.69	3.02	2.26	0.736	2.71	3.57	0.519	1.485
10-Nitrooleate	3.19	1.54	3.375	3.75	2.22	1.05	5.71	13.1	0.928	7.94	3.09	0.976	7.58	7.23	2.71	2.834
PGE3	0.167	0.665	0.45375	0.163	0.00609	1.09	1.09	0.332	0.258	1.78	0.43	0.288	0.451	0.781		0.431
LTE4																
LTB4																
LTB5																
Resolvin D1																
12_13-DiHODE																
14_15-DiHETE																
17(18)-EpETE																
14(15)-EpETE																
11(12)-EpETE																
16(17)-EpDPE																
15-HpETE screen																
12-HpETE screen																
5-HpETE screen																
9-Nitrooleate																
10-Nitrolinoleate																
PGF3a																
MS_METABOLITE_DATA_END
#METABOLITES
METABOLITES_START
metabolite_name	retention index	quantified m/z	PubChem ID	KEGG ID	CID
10-Nitrooleate
9-Nitrooleate
10-Nitrolinoleate
6-keto PGF1a				C05961	5280888
TXB2					5283137
PGE1				C04741	5280723
PGE2				C00584	5280360
15-Keto PGE2
PGD2				C00696	448457
15-deoxy PGJ2				C14717	5311211
PGF2a					53481911
11-HETE					5312981
Lipoxin A4				C06314	5280914
6-trans-LTB4					5283128
5_15-DiHETE					5283158
8_15-DiHETE					53480358
9_12_13-TriHOME				C14833	9858729
9_10-e-DiHO					441460
12_13-DiHOME				C14829	10236635
9_10-DiHOME				C14828	9966640
15_16-DiHODE					16061068
9_10-DiHODE					16061066
14_15-DiHETrE				C14775	5283147
11_12-DiHETrE				C14774	5283146
8_9-DiHETrE				C14773	5283144
5_6-DiHETrE				C14772	5283142
17_18-DiHETE					16061120
19_20-DiHDoPA					16061148
13-HODE				C14762	6443013
9-HODE					5282945
13-HOTE					10469728
9-HOTE					53480359
20-HETE					35027640
15-HETE				C04742	5280724
12-HETE					5312983
9-HETE					5312978
8-HETE				C14776	5283154
5-HETE				C04805	5280733
15-HEPE					53480357
12-HEPE					10041593
9-HEPE					5283187
5-HEPE					6439678
17-HDoHE					6439179
14-HDoHE					11566378
4-HDoHE					11566378
9_10-EpO					15868
12(13)-EpOME					5356421
9(10)-EpOME				C14828	9966640
12(13)-Ep-9-KODE
15(16)-EpODE					16061062
12(13)-EpODE					16061061
9(10)-EpODE					16061060
14(15)-EpETrE				C14813	11954058
11(12)-EpETrE
8(9)-EpETrE				C14769	5283203
19(20)-EpDPE					11631565
13-KODE				C14765	6446027
9-KODE				C14766	9839084
15-KETE				C04577	5280701
5-KETE				C14732	5283159
PGE3				C06439	5280937
LTE4					5280749
LTB4				C05961	5280888
LTB5					5283125
Resolvin D1					16061135
12_13-DiHODE					16061067
14_15-DiHETE					16061119
17(18)-EpETE					16061089
14(15)-EpETE					16061088
11(12)-EpETE					16061087
16(17)-EpDPE					14392758
15-HpETE screen				C05966	5280893
12-HpETE screen				C05965	5280892
5-HpETE screen					5283171
PGF3a
METABOLITES_END
#END