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Портал Begell Электронная Бибилиотека e-Книги Журналы Справочники и Сборники статей Коллекции
Journal of Environmental Pathology, Toxicology and Oncology
Импакт фактор: 1.625 5-летний Импакт фактор: 1.63 SJR: 0.402 SNIP: 0.613 CiteScore™: 2.3

ISSN Печать: 0731-8898
ISSN Онлайн: 2162-6537

Выпуски:
Том 40, 2021 Том 39, 2020 Том 38, 2019 Том 37, 2018 Том 36, 2017 Том 35, 2016 Том 34, 2015 Том 33, 2014 Том 32, 2013 Том 31, 2012 Том 30, 2011 Том 29, 2010 Том 28, 2009 Том 27, 2008 Том 26, 2007 Том 25, 2006 Том 24, 2005 Том 23, 2004 Том 22, 2003 Том 21, 2002 Том 20, 2001

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.v20.i1.110
11 pages

Low Doses of Heavy Metals Disrupt Normal Structure and Function of Rat Platelets

Siragam Vinaya Kumar
Environmental Toxicology Laboratory, Department of Zoology, Visva Bharati University,West Bengal, India
Rakhi Bose
Environmental Toxicology Laboratory, Department of Zoology, Visva Bharati University,West Bengal, India
Shelley Bhattacharya
Environmental Toxicology Laboratory, Department of Zoology, Visva Bharati University,West Bengal, India

Краткое описание

Aggregation, an important property of platelets, plays a key role in the coagulation of blood and is potentiated by ADP and adrenaline, whereas cAMP acts as a strong inhibitor. Because of the rise in the heavy metal load in the environment, more studies are necessary to look at its subtle effects in the animal system, wherein platelet structure and function can be targeted. We carried out structural analyses under phase contrast and scanning electronmicroscopy of the platelets prepared from 1/10 LD50 metal-treated rats. After mercury (Hg) and arsenic (As) treatment, the cell margins appeared irregular and wavy, with small pseudopodia-like protrusions from the surface. Cadmium (Cd) treatment caused loss of the general spindle shape, and the platelets assumed a round spongy appearance. All metal treatments effected enhanced collagen-induced aggregation and inhibited ADP and arachidonic acid-induced aggregation, whereas epinephrine accelerated aggregation in Hg and Cd treatment but inhibited aggregation in As treatment. Cd proved a potent inhibitor of phosphodiesterase, increasing the cAMP level in in vitro treatments at equimolar (5, 10, and 20 pmoles) concentrations. The rate of aggregation was enhanced with all the agonists used in in vitro Hg and As treatments, with concomitant reduction in cAMP, while Cd inhibited platelet aggregation. Thus, we can conclude that cytosolic cAMP, which is decreased by the metal-induced inhibition of phosphodiesterase, is a regulator molecule in platelet aggregation. Furthermore, it is also abundantly clear that equimolar doses of metals are not always equitoxic. Therefore, the action of each xenobiotic is not only due to the concentration used but also to the type of xenobiotic depending on its unique mechanism of action.


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