Abstract
Cyhalothrin, a pyrethroid insecticide, induces stress-like symptoms, increases c-fos immunoreactivity in the paraventricular nucleus of the hypothalamus, and decreases innate immune responses in laboratory animals. Macrophages are key elements in cellular immune responses and operate at the tumor-host interface. This study investigated the relationship among cyhalothrin effects on Ehrlich tumor growth, serum corticosterone levels and peritoneal macrophage activity in mice. Three experiments were done with 10 experimental (single gavage administration of 3.0 mg/kg cyhalothrin daily for 7 days) and 10 control (single gavage administration of 1.0 mL/kg vehicle of cyhalothrin preparation daily for 7 days) isogenic BALB/c mice in each experiment. Cyhalothrin i) increased Ehrlich ascitic tumor growth after ip administration of 5.0 x 106 tumor cells, i.e., ascitic fluid volume (control = 1.97 +/- 0.39 mL and experimental = 2.71 +/- 0.92 mL; P < 0.05), concentration of tumor cells/mL in the ascitic fluid (control = 111.95 +/- 16.73 x 106 and experimental = 144.60 +/- 33.18 x 106; P < 0.05), and total number of tumor cells in the ascitic fluid (control = 226.91 +/- 43.22 x 106 and experimental = 349.40 +/- 106.38 x 106; P < 0.05); ii) increased serum corticosterone levels (control = 200.0 +/- 48.3 ng/mL and experimental = 420.0 +/- 75.5 ng/mL; P < 0.05), and iii) decreased the intensity of macrophage phagocytosis (control = 132.3 +/- 19.7 and experimental = 116.2 +/- 4.6; P < 0.05) and oxidative burst (control = 173.7 +/- 40.8 and experimental= 99.58 +/- 41.7; P < 0.05) in vitro in the presence of Staphylococcus aureus. These data provide evidence that cyhalothrin simultaneously alters host resistance to Ehrlich tumor growth, hypothalamic-pituitary-adrenocortical (HPA) axis function, and peritoneal macrophage activity. The results are discussed in terms of data suggesting a link between stress, HPA axis activation and resistance to tumor growth.
Highlights
Experimental and epidemiological evidence shows the relevance of the interactions between stress and changes in immunity
An inescapable foot shock and a psychological stressor generated with the use of a communication box were shown to concomitantly alter stress levels, macrophage activity, and Ehrlich tumor growth in mice [4]; sound stress suppressed the T- and B-cell mediated responses in rats [5]; inescapable foot shocks increased total alveolar cell count in OVA-sensitized rats [6]; individual housing induced an altered immuneendocrine response and, at the same time, decreased resistance to Ehrlich tumor growth [7]; submissive mice displayed more anxiety-like behaviors and decreased macrophage activity, and showed a decrease in resistance to implantation and development of melanoma metastases in their lungs [8]; stress induced by cohabitation with sick partners decreased macrophage activity [9] and dendritic cell phenotype [10]
Www.bjournal.com.br and control data were detected when the basal oxidative burst was measured in peritoneal macrophages taken 24 h after Ehrlich tumor cell inoculation
Summary
Experimental and epidemiological evidence shows the relevance of the interactions between stress and changes in immunity. An inescapable foot shock and a psychological stressor generated with the use of a communication box were shown to concomitantly alter stress levels, macrophage activity, and Ehrlich tumor growth in mice [4]; sound stress suppressed the T- and B-cell mediated responses in rats [5]; inescapable foot shocks increased total alveolar cell count in OVA-sensitized rats [6]; individual housing induced an altered immuneendocrine response and, at the same time, decreased resistance to Ehrlich tumor growth [7]; submissive mice displayed more anxiety-like behaviors and decreased macrophage activity, and showed a decrease in resistance to implantation and development of melanoma metastases in their lungs [8]; stress induced by cohabitation with sick partners decreased macrophage activity [9] and dendritic cell phenotype [10].
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