Reduced rat plasma lysophosphatidylglycerol or lysophosphatidic acid level as a biomarker of aristolochic acid-induced renal and adipose dysfunctions.
OBJECTIVE
Food products and diet pills containing aristolochic acid (AA) are responsible for a rapid progression of nephropathy associated with reduced body weight in human beings. In this study, we investigated the relationship of dietary NaCl and lysophospholipid (LPL) plasma levels to body weight gain in AA-treated rats.


METHODS
Male rats receiving a salt-deficient chow, normal salt chow or high salt chow were injected intraperitoneally daily with AA for 15days. Body weight, visceral fat mass, food intake, levels of LPL in plasma and its synthesized enzyme were investigated.


RESULTS
Body weight gain, visceral fat mass and daily food intake were smaller in AA-treated rats than those of control rats, regardless of dietary salt concentration. AA treatment decreased plasma levels of major lysophosphatidic acid (LPA) molecular species in rats fed the normal or high-salt chow but not the salt-deficient chow, whereas both the plasma lysophospholipase D activity and kidney mRNA level of autotaxin of AA-treated rats fed chow with defined salt concentrations were lower than those of control rats. Plasma levels of major molecular species of lysophosphatidylglycerol (LPG) in AA-treated rat groups fed chow with defined salt concentrations were lower than those of control rats.


CONCLUSIONS
Plasma levels of LPG and LPA seem to be relevant to the reduced body weight gain and fat mass due to AA treatment.
Department of Pharmaceutical Sciences, Kyushu University of Health and Welfare, Japan.
Toshihiko
T
Tsutsumi
Department of Pharmaceutical Health Chemistry, Institute of Health Biosciences, University of Tokushima Graduate School, Japan.
Yoko
Y
Okamoto
Department of Pharmaceutical Health Chemistry, Institute of Health Biosciences, University of Tokushima Graduate School, Japan.
Syougo
S
Yamakawa
Department of Pharmaceutical Sciences, Kyushu University of Health and Welfare, Japan.
Cheng
C
Bingjun
Department of Anatomic Pathology, Prefectural Nobeoka Hospital, Japan.
Akira
A
Ishihara
Department of Pharmaceutical Health Chemistry, Institute of Health Biosciences, University of Tokushima Graduate School, Japan.
Tamotsu
T
Tanaka
Department of Life Sciences, Faculty of Pharmacy, Yasuda Women's University, Japan.
Akira
A
Tokumura
D000273:Adipose Tissue / Q000187:drug effects* / Q000503:physiopathology; D000818:Animals; D034341:Aristolochic Acids / Q000633:toxicity*; D015415:Biomarkers / Q000097:blood*; D001835:Body Weight / Q000187:drug effects; D005247:Feeding Behavior / Q000187:drug effects; D007668:Kidney / Q000187:drug effects* / Q000503:physiopathology; D008246:Lysophospholipids / Q000097:blood*; D008297:Male; D009929:Organ Size / Q000187:drug effects; D010727:Phosphoric Diester Hydrolases / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage; D000099189:Lysophospholipase D
D034341:Aristolochic Acids; D015415:Biomarkers; D008246:Lysophospholipids; D010727:Phosphoric Diester Hydrolases; D012333:RNA, Messenger; D017673:Sodium Chloride, Dietary; D000099189:Lysophospholipase D; C026223:lysophosphatidylglycerol; C000228:aristolochic acid I; C032881:lysophosphatidic acid
Aristolochic acid nephropathy; Body weight loss; Dietary sodium; Lysophosphatidic acid; Lysophosphatidylglycerol; Lysophospholipase D