Abstract
Atrazine, a pre-emergent herbicide in the chloro-s-triazine family, has been widely used in crop lands and often detected in agriculture watersheds, which is considered as a potential threat to human health. Although atrazine and its metabolites showed an elevated incidence of mammary tumors in female Sprague–Dawley (SD) rats, no molecular evidence was found relevant to its carcinogenesis in humans. This study aims to determine whether atrazine could induce the expression of DNA damage response-related proteins in normal human breast epithelial cells (MCF-10A) and to examine the cytotoxicity of atrazine at a molecular level. Our results indicate that a short-term exposure of MCF-10A to an environmentally-detectable concentration of atrazine (0.1 µg/mL) significantly increased the expression of tumor necrosis factor receptor-1 (TNFR1) and phosphorylated Rad17 in the cells. Atrazine treatment increased H2AX phosphorylation (γH2AX) and the formation of γH2AX foci in the nuclei of MCF-10A cells. Atrazine also sequentially elevated DNA damage checkpoint proteins of ATM- and RAD3-related (ATR), ATRIP and phospho-Chk1, suggesting that atrazine could induce DNA double-strand breaks and trigger the DNA damage response ATR-Chk1 pathway in MCF-10A cells. Further investigations are needed to determine whether atrazine-triggered DNA double-strand breaks and DNA damage response ATR-Chk1 pathway occur in vivo.
Highlights
Atrazine, one of the 2-chloro-s-triazine herbicides, is a most-widely used pre- and early-post-emergence pesticide for crop production in the world [1]
The Environmental Protection Agency (EPA) monitors and enforces a maximum contaminant level (MCL) of atrazine at 3.0 μg/L in public drinking water (Safe Drinking Water Act, 1991), a recent United States Department of Agriculture (USDA) study revealed that the annual mean concentration of atrazine had exceeded the MCL in public drinking water sources, and the concentration in groundwater could be as high as 65 μg/L [3]
This research presented the first study to investigate the genotoxicity of atrazine at environmentally-detectable levels in human MCF-10A cells
Summary
One of the 2-chloro-s-triazine herbicides, is a most-widely used pre- and early-post-emergence pesticide for crop production in the world [1]. According to the U.S Environmental Protection Agency (EPA), more than 34 million kg of atrazine are applied each year in the United States alone. The EPA monitors and enforces a maximum contaminant level (MCL) of atrazine at 3.0 μg/L in public drinking water (Safe Drinking Water Act, 1991), a recent United States Department of Agriculture (USDA) study revealed that the annual mean concentration of atrazine had exceeded the MCL in public drinking water sources, and the concentration in groundwater could be as high as 65 μg/L [3]. Atrazine pollution in surface and ground water is a growing health concern. It is generally considered as an endocrine-disrupting compound (EDC), with adverse effects on the central nervous system [4,5,6], endocrine system [7,8,9] and immune system [10,11]. Even though the classification of atrazine as an EDC has been debated [12], a number of adverse consequences on living organisms, including mammal species, have been reported, especially on the reproductive system of rats [8], pigs [13], fish [14]
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