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Pulmonary hypertension induced by drugs and toxins
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
Kim Bouillon, Yola Moride, Lucien Abenhaim, Marc Humbert
Pyrrolizidine is a heterocyclic organic compound that forms the central chemical structure of a variety of alkaloids known collectively as pyrrolizidine alkaloids. They are plant hepatotoxins that can also cause injury to the vasculature of the lungs leading to pulmonary hypertension and right heart failure in animals. They are named differently according to species of plants Crotalaria and Senecio. Monocrotaline is found in C. spectabilis and fulvine in C. fulva (see Fig. 29.3).86 Monocrotaline-induced pulmonary hypertension in rats is a major animal model for the study of pulmonary hypertension. In S. jacobaea, several alkaloids are found, in particular seneciphylline (see Fig. 29.3).86 Leaves and seeds of these plants are used for the preparation of bush teas, which are consumed by indigenous populations for medicinal and other purposes.
Metabolism of carcinogenic pyrrolizidine alkaloids and pyrrolizidine alkaloid N-oxides by rat primary hepatocytes generate the same characteristic DHP-DNA adducts
Published in Journal of Environmental Science and Health, Part C, 2021
Xiaobo He, Qingsu Xia, Qiang Shi, Peter P. Fu
More than 300 pyrrolizidine alkaloids (PAs) and PA N-oxides are known to be common chemical constituents of over 6000 plant species from different botanical families around the world.1–9 Upon metabolism by liver cytochrome 450 enzymes, PAs and PA N-oxides that contain a double bond at C1 and C2 positions of the unsaturated necine base exhibit cytotoxicity, genotoxicity, and tumorigenicity.2,6,9,10 PAs and PA-containing plants are known to induce liver tumors in rodents.5,6 In addition, a number of PA-containing plant extracts, retrorsine N-oxide (isatidine), dehydropyrrolizidine alkaloids (dehydro-PAs), and dehydroretronecine (DHR) have been determined to be rodent carcinogens.5,6,11
Toxicoproteomic assessment of liver responses to acute pyrrolizidine alkaloid intoxication in rats
Published in Journal of Environmental Science and Health, Part C, 2018
Yan-Hong Li, William Chi-Shing Tai, Imran Khan, Cheng Lu, Yao Lu, Wing-Yan Wong, Wood-Yee Chan, Wen-Luan Wendy Hsiao, Ge Lin
Pyrrolizidine alkaloids (PAs) are one of the most significant groups of phytotoxins widely distributed in about 30% of the world's flowering plants.1,2 Hepatotoxic PAs mainly cause liver damage, and particularly damage sinusoidal endothelial cells (SECs) leading to hepatic sinusoidal obstruction syndrome (HSOS) in human and livestock. Since the first documented human outbreak of 80 PA-induced HSOS cases in South Afghanistan in 1920, numerous life-threatening hepatotoxic cases caused by PA exposure, such as the ingestion of PA-producing medicinal herbs, herbal teas, and vegetables, and also more tragically, the unwitting consumption of PA-contaminated foodstuffs have been continuously reported globally.3–7 PAs are ingested from plants and concentrated in milk via cows and goats, in eggs via poultry, and in honey via bees, daily PA exposure especially through food chain contamination results in a high risk of PA poisoning.8–11 Extensive efforts have been made to investigate the progression and mechanisms underlying hepatotoxicity induced by PAs.12–16 However, due to the complexity of pathogenesis, it remains a great challenge to clarify the events responsible for PA intoxication and fully understand the molecular mechanisms leading to PA-induced hepatotoxicity.