Reference

Monocrotaline-induced pulmonary endothelial dysfunction in rats

Monocrotaline-induced pulmonary endothelial dysfunction in rats. Molteni, Agostino; Ward, William F.; Ts'ao, Chung Hsin; Port, Curtis D.; Solliday, Norman H. (Med. Sch., Northwestern Univ., Chicago, IL 60611, USA). Proc. Soc. Exp. Biol. Med., 176(1), 88-94 (English) 1984. CODEN: PSEBAA. ISSN: 0037-9727. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) To study the role of endothelial damage in the pathogenesis of lung injury induced by monocrotaline (I) [315-22-0], 3 functions [angiotensin I-converting enzyme (ACE) [9015-82-1] activity, plasminogen [9001-91-6] activator (PLA) activity, and prostacyclin (PGI2) [35121-78-9] prodn.] assocd. with the pulmonary endothelium were examd., and correlated with pulmonary arterial perfusion and ultrastructure in rats receiving I in their drinking water (20 mg/L) for 1-12 wk. Lung ACE activity increased after 1 wk of I, then decreased steadily from 1 to 6 wk, before plateauing at ~55% of normal. PLA activity in I-treated lungs did not change significantly for the 1st 2 wk, then decreased to 59 and 79% of the control value after 6 and 12 wk, resp. In contrast, PGI2 prodn. 9015-82-1 and 9001-91-6 which are cas registry numbers of substances are two of reagents here. increased progressively, reaching 140 and 270% of the control level after 6 and 12 wk of I treatment, resp. These endothelial functional changes were not accompanied by significant changes in pulmonary arterial perfusion as visualized by 99mTc lung scans. Electron microscopy of I-treated lungs revealed endothelial damage (pervascular and subendothelial edema, degeneration) starting at 1 wk, and inflammatory and hemorrhagic reactions starting at 2 wk. At 6 and 12 wk, I-treated rats also exhibited increased pulmonary arterial wall thickness, right heart enlargement, and cardio- and hepatomegaly. Thus, I-induced pulmonary injury is accompanied, and in some cases preceded, by structural and functional abnormalities in the pulmonary endothelium. .

Evaluation of amino acids, B vitamins and butylated hydroxyanisole as protective agents against pyrrolizidine alkaloid toxicity in rats

Evaluation of amino acids, B vitamins and butylated hydroxyanisole as protective agents against pyrrolizidine alkaloid toxicity in rats. Garrett, B. J.; Cheeke, P. R. (Oregon State Univ., Corvallis, OR 97331, USA). J. Anim. Sci.In this article, certain chemicals are used. Some of their cas registry numbers are 59-30-3 and 50-06-6 , 58(1), 138-44 (English) 1984. CODEN: JANSAG. ISSN: 0021-8812. DOCUMENT TYPE: Journal CA Section: 18 (Animal Nutrition) Section cross-reference(s): 1, 4 Supplementation of the diets of rats with branched chain amino acids (BCAA: leucine, isoleucine, valine) did not alter their susceptibility to chronic poisoning by tansy ragwort (Senecio jacobaea), which contains hepatotoxic pyrrolizidine alkaloids (PA). Phenobarbital [50-06-6] in the diet, which alters liver microsomal enzyme activity, also did not alter susceptibility to PA poisoning. A combination of BHA [25013-16-5], cysteine [52-90-4], and BCAA did increase survival time of rats fed tansy ragwort. Dietary BHA and cysteine increased the survival time of rats injected with the PA monocrotaline [315-22-0], with evidence that addn. of vitamin B12 [68-19-9] and folic acid [59-30-3] improved the effectiveness of this treatment. In a chronic feeding trial with tansy ragwort, a combination of BHA and cysteine increased the survival times of rats, showing protective activity against PA poisoning. A mixt. of B-complex vitamins, or vitamin B12-folic acid, was not effective in improving the response. .