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In phosphate buffer, the degradation of ATZ by ozone/(O[sub.3]/H[sub.2]O[sub.2]) under various circumstance was explored and the degradation mechanism and dynamics were probed. The findings revealed that when maintaining the reaction temperature at 25 °C, the H[sub.2]O[sub.2] concentration and the O[sub.3] concentration were 20 mol/L and 20 mol/L, respectively. Moreover, the degradation rate of 5 mol/L ATZ under the influence of O[sub.3]/H[sub.2]O[sub.2] was 92.59% in phosphate buffer at pH7. The mechanism analysis showed that HO• and O[sub.3] underwent co-oxidized degradation and that the HO• and O[sub.3] oxidation degradation ratios were close to 1:1 under acidic conditions. Furthermore, HO• oxidative degradation dominated the ATZ degradation process. The kinetics analysis showed that the ATZ kinetics of O[sub.3]/H[sub.2]O[sub.2] degradation were more compatible with quasi-second-order reaction kinetics under different temperatures, pH values, and H[sub.2]O[sub.2] concentrations.

This review was undertaken because it is known that high doses of atrazine activate the HPA axis, leading to increased corticosterone secretion, which could result in immunosuppression.  The mammalian immunotoxicity of atrazine was evaluated based on and studies and the association between chlorotriazine use and the risk of cancer in humans based on epidemiological studies. studies reported that μM concentrations of atrazine may adversely affect cytokine production, lymphocytes, and dendritic cell function. However, there were no consistent patterns of effects of the chlorotriazines on the developing or mature immune system in sub-chronic, chronic, and lifetime animal studies. In a detailed immunotoxicity study on atrazine in rats, there were no effects of atrazine treatment on T-cell-dependent, IgM antibody production or natural killer cell activity. Based on the compendium of toxicology data reviewed, it was concluded that atrazine is unlikely to be immunotoxic at any dose to which humans might realistically be exposed. This conclusion was supported by epidemiological studies indicating that there was no consistent association between occupational exposure to atrazine and cancers of the immune system.

Background: Despite evidence of atrazine toxicity in developing organisms from experimental studies, few studies—and fewer epidemiologic investigations—have examined the potential effects of prenatal exposure. Objectives: We assessed the association between adverse birth outcomes and urinary biomarkers of prenatal atrazine exposure, while taking into account exposures to other herbicides used on corn crops (simazine, alachlor, metolachlor, and acetochlor). Methods: This study used a case-cohort design nested in a prospective birth cohort conducted in the Brittany region of France from 2002 through 2006. We collected maternal urine samples to examine pesticide exposure biomarkers before the 19th week of gestation. Results: We found quantifiable levels of atrazine or atrazine mercapturate in urine samples from 5.5% of 579 pregnant women, and dealkylated and identified hydroxylated triazine metabolites in 20% and 40% of samples, respectively. The presence versus absence of quantifiable levels of atrazine or a specific atrazine metabolite was associated with fetal growth restriction [odds ratio (OR) = 1.5; 95% confidence interval (CI), 1.0-2.2] and small head circumference for sex and gestational age (OR = 1.7; 95% CI, 1.0-2.7). Associations with major congenital anomalies were not evident with atrazine or its specific metabolites. Head circumference was inversely associated with the presence of quantifiable urinary metolachlor. Conclusions: Ulis study is the first to assess associations of birth outcomes with multiple urinary biomarkers of exposure to triazine and chloroacetanilide herbicides. Evidence of associations with adverse birth outcomes raises particular concerns for countries where atrazine is still in use.

Microbial communities play a vital role in biogeochemical cycles, allowing the biodegradation of a wide range of pollutants. The composition of the community and the interactions between its members affect degradation rate and determine the identity of the final products. Here, we demonstrate the application of sequencing technologies and metabolic modeling approaches towards enhancing biodegradation of atrazine—a herbicide causing environmental pollution. Treatment of agriculture soil with atrazine is shown to induce significant changes in community structure and functional performances. Genome-scale metabolic models were constructed for Arthrobacter , the atrazine degrader, and four other non-atrazine degrading species whose relative abundance in soil was changed following exposure to the herbicide. By modeling community function we show that consortia including the direct degrader and non-degrader differentially abundant species perform better than Arthrobacter alone. Simulations predict that growth/degradation enhancement is derived by metabolic exchanges between community members. Based on simulations we designed endogenous consortia optimized for enhanced degradation whose performances were validated in vitro and biostimulation strategies that were tested in pot experiments. Overall, our analysis demonstrates that understanding community function in its wider context, beyond the single direct degrader perspective, promotes the design of biostimulation strategies.

Previous research reported the first case of resistance to mesotrione and other 4-hydroxyphenylpyruvate dioxygenase (HPPD) herbicides in a waterhemp (Amaranthus tuberculatus) population designated MCR (for McLean County mesotrione- and atrazine-resistant). Herein, experiments were conducted to determine if target site or nontarget site mechanisms confer mesotrione resistance in MCR. Additionally, the basis for atrazine resistance was investigated in MCR and an atrazine-resistant but mesotrione-sensitive population (ACR for Adams County mesotrione-sensitive but atrazine-resistant). A standard sensitive population (WCS for Wayne County herbicide-sensitive) was also used for comparison. Mesotrione resistance was not due to an alteration in HPPD sequence, HPPD expression, or reduced herbicide absorption. Metabolism studies using whole plants and excised leaves revealed that the time for 50% of absorbed mesotrione to degrade in MCR was significantly shorter than in ACR and WCS, which correlated with previous phenotypic responses to mesotrione and the quantity of the metabolite 4-hydroxy-mesotrione in excised leaves. The cytochrome P450 monooxygenase inhibitors malathion and tetcyclacis significantly reduced mesotrione metabolism in MCR and corn (Zea mays) excised leaves but not in ACR. Furthermore, malathion increased mesotrione activity in MCR seedlings in greenhouse studies. These results indicate that enhanced oxidative metabolism contributes significantly to mesotrione resistance in MCR. Sequence analysis of atrazine-resistant (MCR and ACR) and atrazine-sensitive (WCS) waterhemp populations detected no differences in the psbA gene. The times for 50% of absorbed atrazine to degrade in corn, MCR, and ACR leaves were shorter than in WCS, and a polar metabolite of atrazine was detected in corn, MCR, and ACR that cochromatographed with a synthetic atrazine-glutathione conjugate. Thus, elevated rates of metabolism via distinct detoxification mechanisms contribute to mesotrione and atrazine resistance within the MCR population.

The herbicide atrazine is widely used across the globe, which is a great concern. To investigate its potential toxicity in the human body, human serum albumin (HSA) was selected as a model protein. The interaction between atrazine and HSA was investigated using steady-state fluorescence spectroscopy, synchronous fluorescence spectroscopy, UV-Vis spectroscopy, three-dimensional (3D) fluorescence spectroscopy and circular dichroism (CD) spectroscopy. The intrinsic fluorescence of HSA was quenched by the atrazine through a static quenching mechanism. Fluorescence spectra at two excitation wavelengths (280 and 295 nm) showed that the fluorescence quenched in HSA was mainly contributed to by tryptophan residues. In addition, the atrazine bound to HSA, which induced changes in the conformation and secondary structure of HSA and caused an energy transfer. Thermodynamic parameters revealed that this binding is spontaneous. Moreover, electrostatic interactions play a major role in the combination of atrazine and HSA. One atrazine molecule can only bind to one HSA molecule to form a complex, and the atrazine molecule is bound at site II (subdomain IIIA) of HSA. This study furthers the understanding of the potential effects posed by atrazine on humans at the molecular level.

Background: exposure to environmental contaminants has been linked to an increased risk of neurological diseases and poor outcomes. Chemical name of Atrazine (ATR) is 6-chloro-N-ethyl-N′-(1-methylethyl)-1,3,5-triazine-2,4-diamine, and it is the most commonly used broad-spectrum herbicide in agricultural crops. Several studies have demonstrated that ATR has the potential to be harmful to the brain’s neuronal circuits. Until today nobody has explored the effect of ATR inhalation on young and aged mice. Methods: young and aged mice were subject to 25 mg of ATR in a vehicle made with saline and 10% of Dimethyl sulfoxide (DMSO) every day for 28 days. At the end of experiment different behavioral test were made and brain was collected. Results: exposure to ATR induced the same response in terms of behavioral alterations and motor and memory impairment in mice but in aged group was more marked. Additionally, in both young and aged mice ATR inhalations induced oxidative stress with impairment in physiological antioxidant response, lipid peroxidation, nuclear factor kappa-light-chain-enhancer of activated B cells (nf-κb) pathways activation with consequences of pro-inflammatory cytokines release and apoptosis. However, the older group was shown to be more sensitive to ATR inhalation. Conclusions: our results showed that aged mice were more susceptible compared to young mice to air pollutants exposure, put in place a minor physiologically response was seen when exposed to it.

This study focused on strategically employing the carboxylesterase enzyme Ha006a, derived from the pesticide-resistant microorganism Helicoverpa armigera, to detect atrazine. A comprehensive analysis through biochemical, biophysical and bioinformatics approaches was conducted to determine the interaction between the Ha006a protein and the herbicide atrazine. These experimental findings elucidated the potential of leveraging the inherent pesticide sequestration mechanism of the Ha006a enzyme for sensor fabrication. Numerous optimizations were undertaken to ensure the precision, reproducibility and convenient storage of the resulting electrochemical sensor, Ha006a/MCPE. This biosensor exhibited exceptional performance in detecting atrazine, demonstrating outstanding selectivity with a lower limit of detection of 5.4 µM. The developed biosensor has emerged as a reliable and cost-effective green tool for the detection of atrazine from diverse environmental samples. The Ha006a-based biosensor fabrication has expanded the possibilities for the efficient integration of insect enzymes as analytical tools, paving the way for the design of cost-effective biosensors capable of detecting and quantifying pesticides.

This study evaluated the toxicity of herbicide atrazine, along with its bioaccumulation and biodegradation in the green microalga Chlamydomonas mexicana. At low concentration (10 μg L⁻¹), atrazine had no profound effect on the microalga, while higher concentrations (25, 50, and 100 μg L⁻¹) imposed toxicity, leading to inhibition of cell growth and chlorophyll a accumulation by 22 %, 33 %, and 36 %, and 13 %, 24 %, and 27 %, respectively. Atrazine 96-h EC50 for C. mexicana was estimated to be 33 μg L⁻¹. Microalga showed a capability to accumulate atrazine in the cell and to biodegrade the cell-accumulated atrazine resulting in 14–36 % atrazine degradation at 10–100 μg L⁻¹. Increasing atrazine concentration decreased the total fatty acids (from 102 to 75 mg g⁻¹) and increased the unsaturated fatty acid content in the microalga. Carbohydrate content increased gradually with the increase in atrazine concentration up to 15 %. This study shows that C. mexicana has the capability to degrade atrazine and can be employed for the remediation of atrazine-contaminated streams.

Synthetic biology enables the reprogramming of cells for useful applications. RNA selection approaches yielded an atrazine-binding riboswitch that was used to engineer Escherichia coli that migrate toward and catabolize this common herbicide. A major goal of synthetic biology is to reprogram cells to perform complex tasks. Here we show how a combination of in vitro and in vivo selection rapidly identifies a synthetic riboswitch that activates protein translation in response to the herbicide atrazine. We further demonstrate that this riboswitch can reprogram bacteria to migrate in the presence of atrazine. Finally, we show that incorporating a gene from an atrazine catabolic pathway allows these cells to seek and destroy atrazine.