Diazinon immunotoxicity in mice: Modulation of cytokines level and their gene expression

Alluwaimi, Ahmed M.; Hussein, Yehia A.

doi:10.1016/j.tox.2007.04.004

Cited by 48 publications

(18 citation statements)

References 19 publications

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“…3(AeF). These results were similar to what has been found that IFN-g2b mRNA synthesis was increased significantly in B cells, CD4þ cells and CD8þ cells of mice after exposure of Diazinon [32]. However, our studies demonstrated that continuing exposure to high levels of ATR and CPF, IFN-g2b mRNA synthesis was reduced, as shown in Fig.…”

Section: Discussionsupporting

confidence: 92%

Effects of atrazine and chlorpyrifos on the mRNA levels of IL-1 and IFN-γ2b in immune organs of common carp

Wang¹,

Xing²,

Li³

et al. 2011

Fish & Shellfish Immunology

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Section: Discussionsupporting

confidence: 92%

Effects of atrazine and chlorpyrifos on the mRNA levels of IL-1 and IFN-γ2b in immune organs of common carp

Wang¹,

Xing²,

Li³

et al. 2011

Fish & Shellfish Immunology

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“…Among these factors, cytokines are considered to be important markers of immune system disturbances that are inflicted by pesticide in the mice. For example, Alluwaimi and Hussein () demonstrated that diazinon immunotoxicity in mice was capable of modulating the major cytokines involved in the regulation of immune responses. Kim et al () reported that treatment of simazine to mice decreased production of cytokines such as IL1, IL6, and TNFα by macrophages.…”

Section: Discussionmentioning

confidence: 99%

Exposure to bifenthrin causes immunotoxicity and oxidative stress in male mice

Jin

Pan²,

Fu³

2012

Environmental Toxicology

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Bifenthrin (BF) is one of the most commonly used pesticides among the synthetic pyrethroids. The effects of BF exposure on the induction of immunotoxicity and oxidative stress were studied both in adolescent and adult male ICR mice. Both the weights of the spleen and thymus decreased significantly in the adolescent mice when they were treated with 20 mg/kg BF for 3 weeks. We found that the 3-week oral administration of BF during puberty increased the transcriptional levels of the genes TNF and IL2 in the spleen and IL2 as well as IL4 in the thymus. The effect of BF exposure on the induction of oxidative stress was also studied in serum and liver samples. The total antioxidant capacity and activity of superoxide dismutase were altered significantly in the serum of the 20 mg/kg BF-treated adolescent mice, and the activity of glutathione peroxidase (GPX) decreased significantly in the serum of adolescent and adult mice after 3 weeks of oral administration of 20 mg/kg BF. Compared to serum, hepatic GSH content increased significantly in both the adolescent and adult mice exposed to 20 mg/kg BF; hepatic CAT and GPX activities were altered significantly, even in adolescent mice, after treatment with 10 mg/kg BF. Taken together, the results of this study suggest that exposure to BF, especially during puberty, has the potential to induce immunotoxicity accompanied by oxidative stress in male mice. These findings will help in elucidating the mechanism of toxicity induced by BF in mice.

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“…The authors provided evidence that lipid peroxidation is due to ROS, produced by the exposed cells. Alluwaimi and Hussein [74] studied the cellular and humoral immune responses to the organophosphate pesticide diazinon and found gradual changes in the levels of various cytokines in diazinon-intoxicated mice. Singh and Jiang [75] found that chronic low level exposure to acephate (ACE), an organophosphate insecticide, impairs the response to LPS in rats.…”

Section: Organophosphate Pesticides Dioxin and Wood Preservationmentioning

confidence: 99%

Role of the Toll Like Receptor (TLR) Radical Cycle in Chronic Inflammation: Possible Treatments Targeting the TLR4 Pathway

Lucas¹,

2013

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Activation of the Toll-like receptor 4 (TLR4) complex, a receptor of the innate immune system, may underpin the pathophysiology of many human diseases, including asthma, cardiovascular disorder, diabetes, obesity, metabolic syndrome, autoimmune disorders, neuroinflammatory disorders, schizophrenia, bipolar disorder, autism, clinical depression, chronic fatigue syndrome, alcohol abuse, and toluene inhalation. TLRs are pattern recognition receptors that recognize damage-associated molecular patterns and pathogen-associated molecular patterns, including lipopolysaccharide (LPS) from gram-negative bacteria. Here we focus on the environmental factors, which are known to trigger TLR4, e.g., ozone, atmosphere particulate matter, long-lived reactive oxygen intermediate, pentachlorophenol, ionizing radiation, and toluene. Activation of the TLR4 pathways may cause chronic inflammation and increased production of reactive oxygen and nitrogen species (ROS/RNS) and oxidative and nitrosative stress and therefore TLR-related diseases. This implies that drugs or substances that modify these pathways may prevent or improve the abovementioned diseases. Here we review some of the most promising drugs and agents that have the potential to attenuate TLR-mediated inflammation, e.g., anti-LPS strategies that aim to neutralize LPS (synthetic anti-LPS peptides and recombinant factor C) and TLR4/MyD88 antagonists, including eritoran, CyP, EM-163, epigallocatechin-3-gallate, 6-shogaol, cinnamon extract, N-acetylcysteine, melatonin, and molecular hydrogen. The authors posit that activation of the TLR radical (ROS/RNS) cycle is a common pathway underpinning many "civilization" disorders and that targeting the TLR radical cycle may be an effective method to treat many inflammatory disorders.

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Diazinon immunotoxicity in mice: Modulation of cytokines level and their gene expression

Cited by 48 publications

References 19 publications

Effects of atrazine and chlorpyrifos on the mRNA levels of IL-1 and IFN-γ2b in immune organs of common carp

Effects of atrazine and chlorpyrifos on the mRNA levels of IL-1 and IFN-γ2b in immune organs of common carp

Exposure to bifenthrin causes immunotoxicity and oxidative stress in male mice

Role of the Toll Like Receptor (TLR) Radical Cycle in Chronic Inflammation: Possible Treatments Targeting the TLR4 Pathway

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