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Oral Exposure to Atrazine Induces Oxidative Stress and Calcium Homeostasis Disruption in Spleen of Mice

View Article: PubMed Central - PubMed

ABSTRACT

The widely used herbicide atrazine (ATR) can cause many adverse effects including immunotoxicity, but the underlying mechanisms are not fully understood. The current study investigated the role of oxidative stress and calcium homeostasis in ATR-induced immunotoxicity in mice. ATR at doses of 0, 100, 200, or 400 mg/kg body weight was administered to Balb/c mice daily for 21 days by oral gavage. The studies performed 24 hr after the final exposure showed that ATR could induce the generation of reactive oxygen species in the spleen of the mice, increase the level of advanced oxidation protein product (AOPP) in the host serum, and cause the depletion of reduced glutathione in the serum, each in a dose-related manner. In addition, DNA damage was observed in isolated splenocytes as evidenced by increase in DNA comet tail formation. ATR exposure also caused increases in intracellular Ca2+ within splenocytes. Moreover, ATR treatment led to increased expression of genes for some antioxidant enzymes, such as HO-1 and Gpx1, as well as increased expression of NF-κB and Ref-1 proteins in the spleen. In conclusion, it appears that oxidative stress and disruptions in calcium homeostasis might play an important role in the induction of immunotoxicity in mice by ATR.

No MeSH data available.


DNA damage in splenocytes. Mice were exposed by daily oral gavage to ATR doses for 21 days. Cells were harvested 24 hr after the final dosing. Representative images of ATR-induced DNA damage in splenocytes. Typical comets are shown in groups nontreated and treated with ATR (400 mg/kg). Magnification = 200x.
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fig5: DNA damage in splenocytes. Mice were exposed by daily oral gavage to ATR doses for 21 days. Cells were harvested 24 hr after the final dosing. Representative images of ATR-induced DNA damage in splenocytes. Typical comets are shown in groups nontreated and treated with ATR (400 mg/kg). Magnification = 200x.

Mentions: Table 3 presents results concerning levels of DNA damage in splenocytes of mice treated with different doses of ATR for 21 days. Figure 5 presents a representative fluorescent figure used in the analyses. The % Tail DNA, tail moment, and Olive tail moment observed at each dose of ATR were all greater than those seen with cells from control mice. Specifically in the cells of mice in the 400 mg/kg group, statistically significant increases in % Tail DNA (12.47-fold increase), tail length (18.85-fold increase), tail moment (229.4-fold increase), and Olive tail moment (47.79-fold increase) were seen.


Oral Exposure to Atrazine Induces Oxidative Stress and Calcium Homeostasis Disruption in Spleen of Mice
DNA damage in splenocytes. Mice were exposed by daily oral gavage to ATR doses for 21 days. Cells were harvested 24 hr after the final dosing. Representative images of ATR-induced DNA damage in splenocytes. Typical comets are shown in groups nontreated and treated with ATR (400 mg/kg). Magnification = 200x.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC5121465&req=5

fig5: DNA damage in splenocytes. Mice were exposed by daily oral gavage to ATR doses for 21 days. Cells were harvested 24 hr after the final dosing. Representative images of ATR-induced DNA damage in splenocytes. Typical comets are shown in groups nontreated and treated with ATR (400 mg/kg). Magnification = 200x.
Mentions: Table 3 presents results concerning levels of DNA damage in splenocytes of mice treated with different doses of ATR for 21 days. Figure 5 presents a representative fluorescent figure used in the analyses. The % Tail DNA, tail moment, and Olive tail moment observed at each dose of ATR were all greater than those seen with cells from control mice. Specifically in the cells of mice in the 400 mg/kg group, statistically significant increases in % Tail DNA (12.47-fold increase), tail length (18.85-fold increase), tail moment (229.4-fold increase), and Olive tail moment (47.79-fold increase) were seen.

View Article: PubMed Central - PubMed

ABSTRACT

The widely used herbicide atrazine (ATR) can cause many adverse effects including immunotoxicity, but the underlying mechanisms are not fully understood. The current study investigated the role of oxidative stress and calcium homeostasis in ATR-induced immunotoxicity in mice. ATR at doses of 0, 100, 200, or 400 mg/kg body weight was administered to Balb/c mice daily for 21 days by oral gavage. The studies performed 24 hr after the final exposure showed that ATR could induce the generation of reactive oxygen species in the spleen of the mice, increase the level of advanced oxidation protein product (AOPP) in the host serum, and cause the depletion of reduced glutathione in the serum, each in a dose-related manner. In addition, DNA damage was observed in isolated splenocytes as evidenced by increase in DNA comet tail formation. ATR exposure also caused increases in intracellular Ca2+ within splenocytes. Moreover, ATR treatment led to increased expression of genes for some antioxidant enzymes, such as HO-1 and Gpx1, as well as increased expression of NF-κB and Ref-1 proteins in the spleen. In conclusion, it appears that oxidative stress and disruptions in calcium homeostasis might play an important role in the induction of immunotoxicity in mice by ATR.

No MeSH data available.