TY - JOUR
T1 - Allylamine and β-aminopropionitrile-induced vascular injury
T2 - Enhanced expression of high-molecular-weight proteins
AU - Awasthi, Sita
AU - Boor, Paul J.
N1 - Funding Information:
Received 20 December 1996; sent for revision 6 February 1997; accepted 14 April 1997. This work was supported by National Institutes of Health grant HL-26189 from the National Heart, Lung, and Blood Institute. The expert secretarial assistance of Judi Bailes is gratefully acknowledged. Address correspondence to Paul J. Boor, Chemical Pathology Division, Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555-0609, USA.
PY - 1998/1
Y1 - 1998/1
N2 - In the present study we describe changes in aorta at the protein level associated with allylamine (AA) and β-aminopropionitrile (βAPN) induced vascular toxicity in a rat model. This model represents a remarkable synergistic, necrotizing toxic effect of these combined toxins, and our rationale was to examine protein expression in order to shed light on the mechanisms underlying this synergism. Rats were given AA (100 mg kg body weight day) and βAPN (1 g kg body weight day) by gavage for 10 d; this protocol has been shown to result in smooth-muscle necrosis, but no visible connective tissue changes. Soluble and insoluble fractions from AA + βAPN- or from βAPN-treated aorta showed enhanced expression of three high-molecular-weight protein bands (ranges between approximately 120 and 95 kD). The time course of induction of proteins showed the appearance of AA + βAPN-induced specific proteins at d 3 of AA + βAPN treatment. Partial purification and characterization suggested that AA + βAPN specific proteins are likely to be collagen proteins (type I). Thus, the data presented in this article help in understanding the vascular toxicity induced by AA + βAPN or by βAPN, in that we have described an altered phenotypic expression of collagenous proteins indicative of selective medial vascular toxicity.
AB - In the present study we describe changes in aorta at the protein level associated with allylamine (AA) and β-aminopropionitrile (βAPN) induced vascular toxicity in a rat model. This model represents a remarkable synergistic, necrotizing toxic effect of these combined toxins, and our rationale was to examine protein expression in order to shed light on the mechanisms underlying this synergism. Rats were given AA (100 mg kg body weight day) and βAPN (1 g kg body weight day) by gavage for 10 d; this protocol has been shown to result in smooth-muscle necrosis, but no visible connective tissue changes. Soluble and insoluble fractions from AA + βAPN- or from βAPN-treated aorta showed enhanced expression of three high-molecular-weight protein bands (ranges between approximately 120 and 95 kD). The time course of induction of proteins showed the appearance of AA + βAPN-induced specific proteins at d 3 of AA + βAPN treatment. Partial purification and characterization suggested that AA + βAPN specific proteins are likely to be collagen proteins (type I). Thus, the data presented in this article help in understanding the vascular toxicity induced by AA + βAPN or by βAPN, in that we have described an altered phenotypic expression of collagenous proteins indicative of selective medial vascular toxicity.
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U2 - 10.1080/009841098159475
DO - 10.1080/009841098159475
M3 - Article
C2 - 9447229
AN - SCOPUS:21544437424
SN - 1528-7394
VL - 53
SP - 61
EP - 76
JO - Journal of Toxicology and Environmental Health - Part A
JF - Journal of Toxicology and Environmental Health - Part A
IS - 1
ER -