Early kidney damage induced by subchronic exposure to PM2.5 in rats
| Autor: | Olivier Barbier, M. Uribe-Ramírez, O.G. Aztatzi-Aguilar, A. De Vizcaya-Ruiz, Juana Narváez-Morales |
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| Rok vydání: | 2016 |
| Předmět: |
Male
0301 basic medicine medicine.medical_specialty Health Toxicology and Mutagenesis Bradykinin Renal function Inflammation 010501 environmental sciences Biology Kidney Toxicology medicine.disease_cause 01 natural sciences Rats Sprague-Dawley 03 medical and health sciences chemistry.chemical_compound Internal medicine Renin–angiotensin system medicine Animals 0105 earth and related environmental sciences Lung medicine.diagnostic_test Research Antioxidant response Angiotensin and bradykinin systems General Medicine Rats Cardiovascular diseases 030104 developmental biology Bronchoalveolar lavage medicine.anatomical_structure Endocrinology Kidney biomarkers chemistry Cytokines Particulate Matter medicine.symptom Bronchoalveolar Lavage Fluid Oxidative stress |
| Zdroj: | Particle and Fibre Toxicology |
| ISSN: | 1743-8977 |
| DOI: | 10.1186/s12989-016-0179-8 |
| Popis: | Background Particulate matter exposure is associated with respiratory and cardiovascular system dysfunction. Recently, we demonstrated that fine particles, also named PM2.5, modify the expression of some components of the angiotensin and bradykinin systems, which are involved in lung, cardiac and renal regulation. The endocrine kidney function is associated with the regulation of angiotensin and bradykinin, and it can suffer damage even as a consequence of minor alterations of these systems. We hypothesized that exposure to PM2.5 can contribute to early kidney damage as a consequence of an angiotensin/bradykinin system imbalance, oxidative stress and/or inflammation. Results After acute and subchronic exposure to PM2.5, lung damage was confirmed by increased bronchoalveolar lavage fluid (BALF) differential cell counts and a decrease of surfactant protein-A levels. We observed a statistically significant increment in median blood pressure, urine volume and water consumption after PM2.5 exposure. Moreover, increases in the levels of early kidney damage markers were observed after subchronic PM2.5 exposure: the most sensitive markers, β-2-microglobulin and cystatin-C, increased during the first, second, sixth and eighth weeks of exposure. In addition, a reduction in the levels of specific cytokines (IL-1β, IL-6, TNF-α, IL-4, IL-10, INF-γ, IL-17a, MIP-2 and RANTES), and up-regulated angiotensin and bradykinin system markers and indicators of a depleted antioxidant response, were also observed. All of these effects are in concurrence with the presence of renal histological lesions and an early pro-fibrotic state. Conclusion Subchronic exposure to PM2.5 induced an early kidney damage response that involved the angiotensin/bradykinin systems as well as antioxidant and immune imbalance. Our study demonstrates that PM2.5 can induce a systemic imbalance that not only affects the cardiovascular system, but also affects the kidney, which may also overall contribute to PM-related diseases. Electronic supplementary material The online version of this article (doi:10.1186/s12989-016-0179-8) contains supplementary material, which is available to authorized users. |
| Databáze: | OpenAIRE |
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