Pesquisa relaciona aumento do risco de obesidade à contaminação pelo agrotóxico atrazina

Um novo estudo [Chronic Exposure to the Herbicide, Atrazine, Causes Mitochondrial Dysfunction and Insulin Resistance], publicado na PLos One, mostra que ratos submetidos à exposição prolongada ao agrotóxico atrazina tiveram sobrepeso quando alimentados com dieta normal e obesidade quando alimentados com dietas de alto teor de gordura. Estas condições de saúde podem levar à diabetes e podem ser responsáveis por danos às estruturas críticas nas células responsáveis pela elaboração de energia.


Os resultados sugerem um novo mecanismo para explicar resultados de estudos anteriores que encontraram uma associação entre as áreas dos Estados Unidos com pesada aplicação de atrazina e a alta prevalência de obesidade.
Para os primeiros meses de estudo os ratos expostos à atrazina e alimentados com dieta normal pesaram o mesmo. No entanto, ao final do estudo, os ratos alimentados com a dieta normal, expostos à água potável com resíduos de atrazina, ficaram 5% mais pesados do que os ratos não expostos ao agrotóxico. Os ratos expostos à atrazina, que foram alimentados com a dieta com alto teor de gordura ficaram 10% mais pesados do que os que não foram expostos mas que foram alimentados com a mesma dieta com alto teor de gordura.

Não foram observadas diferenças no consumo alimentar e no nível de atividade entre os grupos de ratos.

A gordura visceral, ou a gordura que envolve os órgãos do corpo, bem como a gordura dentro dos próprios órgãos, foi a razão para o excesso de peso.

Os ratos expostos à atrazina foram mais resistentes à insulina e os níveis de glicose e insulina em ambos foram significativamente maiores do que nos ratos não expostos à atrazina.

Ensaios de atividade mitocondrial mostrou que a atrazina atuou diretamente , prejudicando o funcionamento das mitocôndrias.

O excesso de gordura em seres humanos é atualmente uma ‘epidemia’ nos Estados Unidos e está associada a doenças cardiovasculares, diabetes e uma série de outros problemas.

Embora as concentrações de atrazina utilizadas neste estudo fossem inferiores aos limites tolerados na água potável (3 microgramas por litro), a dose de baixa concentração utilizada neste estudo foi de mais de 10 mil vezes menor do que a dose necessária para causar efeitos reprodutivos, de acordo com outros estudos em ratos e está no intervalo das doses requeridas para aumentar o risco de câncer em células humanas (Wetzel et al. 1994; Sanderson et al., 2000).


Outras fontes de consulta:

Hayes TB, A Collins, M Lee, M Mendoza, N Noriega, AA Stuart and A Vonk 2002. Hermaphroditic, demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Proceedings of the National Academy of Sciences 99:5476-5480.

National Tap Water Database. Environmental Working Group.

Petersen KF, D Befroy, S Dufour, J Dziura, C Ariyan, DL Rothman, L DiPietro, GW Cline and GI Shulman 2003. Mitochondrial dysfunction in the elderly: possible role in insulin resistance. Science 300:1140-1142.

Sanderson JT, W Seinen, JP Giesy and M van den Berg 2000. 2-chloro-s-triazine herbicides induce aromatase (CYP19) activity in H295R human adrenocortical carcinoma cells: A novel mechanism for estrogenicity? Toxicological Sciences 54:121-127.

Wetzel LT, LG Luempert, CB Breckenridge, MO Tisdel, JT Stevens, AK Thaker, PJ Extrom and JC Eldridge 1994. Chronic effects of atrazine on estrus and mammary-tumor formation in female Sprague-Dawley and Fischer-344 rats. Journal of Toxicology and Environmental Health 43:169-182.

O artigo “Chronic Exposure to the Herbicide, Atrazine, Causes Mitochondrial Dysfunction and Insulin Resistance“, publicado na PLos One, está disponível para acesso integral no formato HTML. Para acessar o artigo clique aqui.

Para maiores informações transcrevemos, abaixo, o abstract:

Chronic Exposure to the Herbicide, Atrazine, Causes Mitochondrial Dysfunction and Insulin Resistance

Soo Lim1, Sun Young Ahn4, In Chan Song2, Myung Hee Chung3, Hak Chul Jang1, Kyong Soo Park1, Ki-Up Lee5, Youngmi Kim Pak4*, Hong Kyu Lee1*

1 Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea, 2 Department of Radiology, Seoul National University College of Medicine, Seoul, Korea, 3 Department of Pharmacology, Seoul National University College of Medicine, Seoul, Korea, 4 Age-Related and Brain Diseases Research Center, Department of Nanopharmaceutical and Life Sciences, Department of Physiology, Kyung Hee University College of Medicine, Seoul, Korea, 5 Department of Internal Medicine, University of Ulsan College of Medicine, Seoul, Korea

Abstract

There is an apparent overlap between areas in the USA where the herbicide, atrazine (ATZ), is heavily used and obesity-prevalence maps of people with a BMI over 30. Given that herbicides act on photosystem II of the thylakoid membrane of chloroplasts, which have a functional structure similar to mitochondria, we investigated whether chronic exposure to low concentrations of ATZ might cause obesity or insulin resistance by damaging mitochondrial function. Sprague-Dawley rats (n = 48) were treated for 5 months with low concentrations (30 or 300 µg kg?1 day?1) of ATZ provided in drinking water. One group of animals was fed a regular diet for the entire period, and another group of animals was fed a high-fat diet (40% fat) for 2 months after 3 months of regular diet. Various parameters of insulin resistance were measured. Morphology and functional activities of mitochondria were evaluated in tissues of ATZ-exposed animals and in isolated mitochondria. Chronic administration of ATZ decreased basal metabolic rate, and increased body weight, intra-abdominal fat and insulin resistance without changing food intake or physical activity level. A high-fat diet further exacerbated insulin resistance and obesity. Mitochondria in skeletal muscle and liver of ATZ-treated rats were swollen with disrupted cristae. ATZ blocked the activities of oxidative phosphorylation complexes I and III, resulting in decreased oxygen consumption. It also suppressed the insulin-mediated phosphorylation of Akt. These results suggest that long-term exposure to the herbicide ATZ might contribute to the development of insulin resistance and obesity, particularly where a high-fat diet is prevalent.

Citation: Lim S, Ahn SY, Song IC, Chung MH, Jang HC, et al. (2009) Chronic Exposure to the Herbicide, Atrazine, Causes Mitochondrial Dysfunction and Insulin Resistance. PLoS ONE 4(4): e5186. doi:10.1371/journal.pone.0005186

Editor: German Malaga, Universidad Peruana Cayetano Heredia, Peru

Received: February 10, 2009; Accepted: February 19, 2009; Published: April 13, 2009

Copyright: © 2009 Lim et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Funding: This work is supported by the IT R&D program of MIC/IITA [2006-S075-01 to HK Lee, Development of an early diagnostic system of metabolic syndrome based on nanosensor integrated network computing], a Korea Science and Engineering Foundation (KOSEF) grant (M10642140004-06N4214-00410 to YK Pak) and a grant from the 21C Frontier Functional Proteomics Project (FPR08A1-070 to YK Pak) from the Ministry of Education, Science & Technology, Korea. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist.

* E-mail: ykpak{at}khu.ac.kr (YKP); hkleemd{at}snu.ac.kr (HKL)

FONTE:  http://www.ecodebate.com.br/2009/05/30/pesquisa-relaciona-aumento-do-risco-de-obesidade-a-contaminacao-pelo-agrotoxico-atrazina/