Target Sites of Fungicides with Primary Effects on Lipid Peroxidation

Edlich, W.; Lyr, H.

doi:10.1201/9781351077088-4

Cited by 11 publications

(4 citation statements)

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“…Due to its low toxicity and high efficiency, PRO is widely used to treat diseases in crops such as fruits and vegetables 22 . The action of PRO is to cause expansion of the budding tubes and hyphae of the spores, which deform the hyphae, thus preventing early spot formation and expansion of the spots 23 . The normal dose of PRO was 0.5–1 kg/ha 24 .…”

Section: Introductionmentioning

confidence: 99%

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Effects of maternal exposure to procymidone on hepatic metabolism in the offspring of mice

Wang

Jin

et al. 2023

Environmental Toxicology

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As an effective fungicide widely used in agricultural production, the excessive procymidone (PRO) residue has been detected in the environment and food. Our previous study demonstrated that PRO could destroy the intestinal barrier in mice and has a joint toxic effect. To explore the cross-generational impact of maternal exposure, 10-week-old C57BL/6 female mice were orally administrated to 10 and 100 mg/kg body weight/day of PRO during pregnancy and lactation. The offspring obtained nutrients from the maternal through the placenta and breast milk, and PRO residues were detected in the liver, intestine, and feces of F1 generation. Fecal examination found that the residual PRO had been completely metabolized when the offspring mice grew to 35 days. The drug residue of F1 generation male mice was higher than that of female mice. We attributed this result to the difference in cytochrome P450 (CYP450) enzyme expression between male and female mice. The transcriptional levels of CYP1A1, CYP1A2, CYP2D9, and CYP3A4, and CYP450 protein expression levels, were higher in female mice. Furthermore, targeted MS of plasma revealed abnormal amino acid levels. In addition, PRO-induced hepatic metabolite changes in F0 and F1-7w mice. KEGG pathway analysis further showed that PRO jointly changed the amino acid biosynthesis pathway of the maternal and offspring. In summary, these results indicated that maternal exposure to PRO during a special period would interfere with self metabolism, and offspring will also have metabolic disorders.

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Section: Introductionmentioning

confidence: 99%

“…22 The action of PRO is to cause expansion of the budding tubes and hyphae of the spores, which deform the hyphae, thus preventing early spot formation and expansion of the spots. 23 The normal dose of PRO was 0.5-1 kg/ha. 24 However, the heavy use of PRO and its high stability has led to residues of PRO in the soil and water environment, and even in food.…”

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confidence: 99%

Effects of maternal exposure to procymidone on hepatic metabolism in the offspring of mice

Wang

Jin

et al. 2023

Environmental Toxicology

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“…Dicarboximide fungicides are known to induce lipid peroxidation in fungi [15], mammalian cells [16], primary cultured trout hepatocytes [17] and impact the human respiratory system in vitro [18]. Procymidone is an endocrine disruptor [19] and it is known to bind the androgen receptor (AR) and acts as an AR antagonist in vivo and in vitro, inhibiting androgen-dependent gene expression by inhibiting AR-binding to DNA [20].…”

Section: Introductionmentioning

confidence: 99%

Short-Term and Long-Term Carcinogenic Effects of Food Contaminants (4-Hydroxynonenal and Pesticides) on Colorectal Human Cells: Involvement of Genotoxic and Non-Genomic Mechanisms

Arnaud

Gauthier

Naour

et al. 2021

Cancers

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To investigate environmental impacts upon colorectal carcinogenesis (CRC) by diet, we assessed two western diet food contaminants: 4-hydroxynonenal (HNE), a major lipid peroxidation product neoformed during digestion, and a mixture of pesticides. We used human colonic cell lines ectopically eliciting varied genetic susceptibilities to CRC: the non-transformed human epithelial colonic cells (HCECs) and their five isogenic cell lines with the loss of APC (Adenomatous polyposis coli) and TP53 (Tumor protein 53) and/or ectopic expression of mutated KRAS (Kristen-ras). These cell lines have been exposed for either for a short time (2 -24 h) or for a long period (3 weeks) to 1 µM HNE and/or 10 µM pesticides. After acute exposure, we did not observe any cytotoxicity or major DNA damage. However, long-term exposure to pesticides alone and in mixture with HNE induced clonogenic transformation in normal HCECs, as well as in cells representing later stages of carcinogenesis. It was associated with genotoxic and non-genomic mechanisms (cell growth, metabolic reprogramming, cell mobility and epithelial-mesenchymal transition) depending on genetic susceptibility. This study demonstrated a potential initiating and promoting effect of food contaminants on CRC after long-term exposure. It supports that these contaminants can accelerate carcinogenesis when mutations in oncogenes or tumor suppressor genes occur.

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“…These compounds can cause protein dysfunction and damage of biomolecules, therefore negatively affecting the pathogen homeostasis (Halliwell and Gutteridge, 2015 ; El-Benna et al, 2016 ). Several fungicides are also able to promote the ROS increase, including OHPs, which are related to fungi annihilation (Edlich and Lyr, 1992 ; Belenky et al, 2013 ; Shekhova et al, 2017 ). On the other hand, some fungal pathogens are able to produce OHPs to protect themselves against invasion and host tissue destruction by other microorganisms (Deighton et al, 1999 ).…”

Section: Introductionmentioning

confidence: 99%

The Human Pathogen Paracoccidioides brasiliensis Has a Unique 1-Cys Peroxiredoxin That Localizes Both Intracellularly and at the Cell Surface

Longo

Breyer

Novaes

et al. 2020

Front. Cell. Infect. Microbiol.

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Paracoccidioides brasiliensis is a temperature-dependent dimorphic fungus that causes systemic paracoccidioidomycosis, a granulomatous disease. The massive production of reactive oxygen species (ROS) by the host's cellular immune response is an essential strategy to restrain the fungal growth. Among the ROS, the hydroperoxides are very toxic antimicrobial compounds and fungal peroxidases are part of the pathogen neutralizing antioxidant arsenal against the host's defense. Among them, the peroxiredoxins are highlighted, since some estimates suggest that they are capable of decomposing most of the hydroperoxides generated in the host's mitochondria and cytosol. We presently characterized a unique P. brasiliensis 1-Cys peroxiredoxin (PbPrx1). Our results reveal that it can decompose hydrogen peroxide and organic hydroperoxides very efficiently. We showed that dithiolic, but not monothiolic compounds or heterologous thioredoxin reductant systems, were able to retain the enzyme activity. Structural analysis revealed that PbPrx1 has an α/β structure that is similar to the 1-Cys secondary structures described to date and that the quaternary conformation is represented by a dimer, independently of the redox state. We investigated the PbPrx1 localization using confocal microscopy, fluorescence-activated cell sorter, and immunoblot, and the results suggested that it localizes both in the cytoplasm and at the cell wall of the yeast and mycelial forms of P. brasiliensis , as well as in the yeast mitochondria. Our present results point to a possible role of this unique P. brasiliensis 1-Cys Prx1 in the fungal antioxidant defense mechanisms.

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Target Sites of Fungicides with Primary Effects on Lipid Peroxidation

Cited by 11 publications

References 0 publications

Effects of maternal exposure to procymidone on hepatic metabolism in the offspring of mice

Effects of maternal exposure to procymidone on hepatic metabolism in the offspring of mice

Short-Term and Long-Term Carcinogenic Effects of Food Contaminants (4-Hydroxynonenal and Pesticides) on Colorectal Human Cells: Involvement of Genotoxic and Non-Genomic Mechanisms

The Human Pathogen Paracoccidioides brasiliensis Has a Unique 1-Cys Peroxiredoxin That Localizes Both Intracellularly and at the Cell Surface

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