| Literature DB >> 31796256 |
Geir Bjørklund1, Lyudmila Pivina2, Maryam Dadar3, Yuliya Semenova2, Md Mostafizur Rahman4, Salvatore Chirumbolo5, Jan Aaseth6.
Abstract
Indications of proximal tubule effects have been observed in recent surveillance study of Gulf War veterans exposed to depleted uranium (DU). This gives some support for the suspicion that DU may represent one of the causes for the so-called Persian Gulf syndrome. Proposed effects may be especially harmful if the toxicity hits the mitochondrial DNA since the mitochondria lack the nucleotide excision repair mechanism, which is needed for repairing bulky adducts that have been associated with DU. It is a plausible working hypothesis that a significant part of the symptoms from various organs, which have been observed among veterans from Gulf War 1 and that have been grouped under the name of the Persian Gulf syndrome, may be explained as a consequence of mitochondrial DNA damage in various cell types and organs. Interpretation of observations, on military personnel and civilians after Gulf War 1, is associated with difficulties because of the abundance of potential confounding factors. The symptoms observed on veterans from Gulf War 1 may be attributed to a multiplicity of substances functioning directly or indirectly as mitochondrial mutagens. A concise analysis of the cascade of toxic effects initiated by DU exposure in the human body is the subject of this article.Entities:
Keywords: Depleted uranium; Gulf war illness; Radiation; Uranium chemical properties; Uranium metabolism; Uranium toxicity
Year: 2019 PMID: 31796256 DOI: 10.1016/j.envres.2019.108927
Source DB: PubMed Journal: Environ Res ISSN: 0013-9351 Impact factor: 6.498