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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.


Flow cytometry analysis of ROS levels in splenocytes. Mice were exposed by daily oral gavage to ATR doses for 21 days. Cells were harvested 24 hr after the final dosing. Values shown are for means ± SE for five mice (males and females combined), analyzed individually. Value is significantly different from control (∗p < 0.05; ∗∗p < 0.01).
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fig2: Flow cytometry analysis of ROS levels in splenocytes. Mice were exposed by daily oral gavage to ATR doses for 21 days. Cells were harvested 24 hr after the final dosing. Values shown are for means ± SE for five mice (males and females combined), analyzed individually. Value is significantly different from control (∗p < 0.05; ∗∗p < 0.01).

Mentions: Analyses of intracellular ROS (Figure 2) indicated that formation of these products was upregulated in a dose-related manner as a result of each of the ATR treatments. Specifically, the mean fluorescence intensity of DCF in ATR treatment groups increased 1.34-, 1.66-, and 2.10-fold compared to the untreated group.


Oral Exposure to Atrazine Induces Oxidative Stress and Calcium Homeostasis Disruption in Spleen of Mice
Flow cytometry analysis of ROS levels in splenocytes. Mice were exposed by daily oral gavage to ATR doses for 21 days. Cells were harvested 24 hr after the final dosing. Values shown are for means ± SE for five mice (males and females combined), analyzed individually. Value is significantly different from control (∗p < 0.05; ∗∗p < 0.01).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig2: Flow cytometry analysis of ROS levels in splenocytes. Mice were exposed by daily oral gavage to ATR doses for 21 days. Cells were harvested 24 hr after the final dosing. Values shown are for means ± SE for five mice (males and females combined), analyzed individually. Value is significantly different from control (∗p < 0.05; ∗∗p < 0.01).
Mentions: Analyses of intracellular ROS (Figure 2) indicated that formation of these products was upregulated in a dose-related manner as a result of each of the ATR treatments. Specifically, the mean fluorescence intensity of DCF in ATR treatment groups increased 1.34-, 1.66-, and 2.10-fold compared to the untreated group.

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&thinsp;mg/kg body weight was administered to Balb/c mice daily for 21 days by oral gavage. The studies performed 24&thinsp;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-&kappa;B 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.