Atrazine alters nitric oxide secretion and cytokines production in LPS-stimulated BalB/c mice, RAW264.7 macrophage and THP-1 cell lines.

Here, we investigated the effect of atrazine (ATZ, 50 mg kg-1 body weight) on lipopolysaccharide (LPS)-induced inducible nitric oxide synthase (iNOS) expression, nitric oxide (NO) production, tissue weights and oxidative stress variables (thiobarbituric acid reactive substances; (TBARS; measured as malondialdehyde) and catalase activity) in the testis, liver, epididymis, and prostate of BALB/c mice. In vitro, we examined the effects of ATZ (1-200 μM) on LPS-induced oxidative stress markers and NO production in RAW 264.7 macrophages, and cytokine responses (tumor necrosis factor-α: TNF-α and interleukin-1β: IL-1β) in differentiated THP-1 human macrophages after 48 h. The liver, testis, and prostate of ATZ + LPS animals had low NO concentrations relative to the LPS values. Interestingly, TBARS was increased in the ATZ + LPS-exposed mice in liver, epididymis and prostate compared to the LPS-treated mice. ATZ + LPS co-exposure also decreased the weight of the testis, epididymis, and prostate and altered the expression of iNOS in all the tissues. In vitro, ATZ alters the responses of RAW264.7 macrophages to inflammatory stimuli (LPS) by suppressing NO production. In differentiated THP-1 human macrophages, ATZ diminished TNF and IL-1β production following LPS stimulation. Altogether, our data indicate that atrazine suppresses immunological response in LPS-stimulated BALB/c mice and macrophage cell lines.