Abstract
Benzophenone-3 is a putative endocrine disrupting chemical and common ingredient in sunscreens. The potential of endocrine disrupting chemicals to act as agonists or antagonists in critical hormonally regulated processes, such as mammary gland development and mammary tumorigenesis, demands evaluation of its potential in promoting breast cancer. This study identifies the effects of BP-3 on mammary tumorigenesis with high-fat diet during puberty versus adulthood in Trp53-null transplant BALB/c mice. Benzophenone-3 exposure yielded levels in urine similar to humans subjected to heavy topical sunscreen exposure. Benzophenone-3 was protective for epithelial tumorigenesis in mice fed lifelong low-fat diet, while promotional for epithelial tumorigenesis in mice fed adult high-fat diet. Benzophenone-3 increased tumor cell proliferation, decreased tumor cell apoptosis, and increased tumor vascularity dependent on specific dietary regimen and tumor histopathology. Even in instances of an ostensibly protective effect, other parameters suggest greater risk. Although benzophenone-3 seemed protective on low-fat diet, spindle cell tumors arising in these mice showed increased proliferation and decreased apoptosis. This points to a need for further studies of benzophenone-3 in both animal models and humans as a potential breast cancer risk factor, as well as a more general need to evaluate endocrine disrupting chemicals in varying dietary contexts.
Highlights
Ovarian hormones are strongly implicated in the etiology of breast cancer [1, 2], and are important for the development of the breast during puberty and young adulthood [3]
As the initial experiment involved relatively longterm treatment with BP-3 and acute exposure to E2, we examined the effects of BP-3 in an acute exposure regimen at our standard dose, as well as 0.1 and 0.01 doses, with and without co-treatment with E2 in OVX pubertal BALB/c mice fed high saturated animal fat diet (HFD)
While BP-3 by itself showed no effects at any dose, BP-3 augmented the proliferative response to E2 in both ducts and duct ends at the standard dose and in duct ends at the 0.1 dose (Figure 1B)
Summary
Ovarian hormones are strongly implicated in the etiology of breast cancer [1, 2], and are important for the development of the breast during puberty and young adulthood [3]. Putative endocrine disrupting chemicals (EDCs), estrogenic chemicals, have emerged as suspects in environmental promotion of breast cancer [4]. Environmental EDCs have the potential to act as agonists or antagonists in critical hormonally regulated processes, such as mammary gland development and mammary tumorigenesis. This warrants evaluation of their potential in promoting breast cancer. Examination of the activity of EDCs in a dietary context may provide additional insight into the potential role of EDCs in promoting breast cancer
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