Di-(2-ethylhexyl) phthalate (DEHP) in the environment and food chain may impact cerebrum development and neurobehavioral in humans and wildlife. However, it is unclear that DEHP exposure caused ...cerebral toxicity. This experiment used gavage to expose female quail to 0, 250, 500, and 1000 mg/kg BW/day for 45 days to assess the potential neurotoxicity of DEHP to the cerebrum. It can be observed that there will be obvious neurological abnormalities in the experiment. Cerebrum histological lesions can be observed with HE-staining. Detecting oxidative stress indices, Nrf2 pathway, and mitochondrial dynamics factor, by analyzing the results, these results were observed that DEHP exposure can cause damage to the cerebrum by causing oxidative stress and affecting the balance of mitochondrial dynamics. Nrf2-mediated defense is not activated by exposure to 250 mg/kg DEHP. Nrf2-mediated defense is activated but is not resistant to exposure to medium and high doses of DEHP (500 mg/kg; 1000 mg/kg). DEHP triggers cerebral mitochondrial dysfunction via modulating mitochondrial dynamics.
DEHP exposure causes cerebral toxicity. DEHP causes oxidative stress in the cerebrum. DEHP regulates oxidative stress by activating the Nrf2 defense response. DEHP exposure also triggers disruption of mitochondrial dynamics leading to mitochondrial damage leading to oxidative stress. Display omitted
•DEHP induces the cerebral toxicity.•DEHP activates Nrf2-mediated antioxidant defense in the cerebrum.•DEHP induced cerebral toxicity via disrupting mitochondrial dynamics.•DEHP triggers mitochondrial dysfunction via modulating mitochondrial dynamics.
The widely used Di-(2-ethylhexyl) phthalate (DEHP) has been reported to exhibit ubiquitous environmental and global health hazards. The bioaccumulation and environmental persistence of DEHP can cause ...serious health hazards in wildlife animals and human. However, DEHP-induced nephrotoxicity in bird is remained unknown. Thus, this study explored the related mechanism of DEHP nephrotoxicity in quail. For this purpose, quail were exposed with DEHP at doses of 0, 250, 500, and 1000 mg/kg body weight daily by gavage administration for 45 days. The results showed that DEHP exposure induced renal injury, oxidative stress, and endoplasmic reticulum (ER) degeneration. Low level DEHP (250 mg/kg) exposure inhibited Nrf2 signaling pathway and induced renal injury via oxidative stress and suppressed the unfolded protein response (UPR) signaling pathway and induced ER stress in the kidney. But surprisingly, high level DEHP (500 mg/kg and 1000 mg/kg) exposure activated Nrf2 and UPR signaling pathways and protected kidney, but they still couldn't resist the toxicity of DEHP. Our study demonstrated that DEHP-induced nephrotoxicity in quail was associated with activating Nrf2-mediated antioxidant defense response and UPR signaling pathway.
DEHP exposure induced renal injury and destroyed the pathophysiological integrity of the kidney in quail. DEHP-induced nephrotoxicity is associated with oxidative stress, which could be regulated by Nrf2-mediated defense response. DEHP exposure activated the UPR signaling pathway to prevent ER stress in the kidney. Display omitted
•DEHP-induced nephrotoxicity is associated with oxidative stress.•DEHP activates Nrf2 signaling pathway in the kidney.•DEHP-induced nephrotoxicity triggers renal ER stress.•DEHP activates UPR in the kidney.•DEHP induces crosstalk between UPR and Nrf2-mediated antioxidant defense in renal injury.
DEHP-induced nephrotoxicity is associated with crosstalk between activated UPR and Nrf2-mediated antioxidant defense mechanism.
Atrazine is well known to be a biologically hazardous substance with toxic effects, but atrazine-induced neurotoxicity remains unclear. The aim of this study was to investigate the mechanisms of ...atrazine-induced cerebellar toxicity. To determine atrazine-exerted potential neurotoxicity, quails were treated with 50, 250 and 500 mg/kg atrazine by gavage administration for 45 days. Notably, the changes of cytochrome P450 enzyme system (CYP450s) were observed in atrazine-exposed quails. The contents of cytochrome P450 (CYP450) and Cytochrome b5 (Cyt b5) and the activities of NADPH-cytochrome c reductase (NCR), aminopyrin N-demethylase (APND) and aniline-4-hydeoxylase (AH) were increased and erythromycin N-demethylase (ERND) was decreased in quail cerebellum. Nuclear xenobiotic receptors (NXRs) and the transcriptions of NXRs-related target molecules were influenced in cerebellum. Atrazine disrupted the CYP450s balance in quail cerebellum. These results suggested that atrazine-induced cerebellar toxicity in birds was associated with activating PXR/CAR pathway responses and disrupting cytochrome P450 homeostasis. This study provided novel evidences that atrazine exposure induced cerebellar toxicity.
Atrazine (ATR) exposure induced the cerebellar toxicity. ATR caused CYP450s disruption in quail cerebellum. ATR regulated the CYP450s homeostasis by activation of NXRs responses and inducing the transcription of the CYP450 isoforms. Display omitted
•Atrazine induces the cerebellar toxicity.•Atrazine triggers the PXR/CAR pathway responses in cerebellum.•Atrazine disrupts the cytochrome P450 homeostasis in cerebellum.•Atrazine impacts the transcription of CYPs via activating the NXRs responses.
Di-(2-ethylhexyl)-phthalate (DEHP) is causing serious health hazard in wildlife animal and human through environment and food chain, including the effect of brain development and impacted ...neurobehavioral outcomes. However, DEHP exposure caused cerebellar toxicity in bird remains unclear. To evaluate DEHP-exerted potential neurotoxicity in cerebellum, male quails were exposed with 0, 250, 500 and 750 mg/kg BW/day DEHP by gavage treatment for 45 days. Neurobehavioral abnormality and cerebellar histopathological alternation were observed in DEHP-induced quails. DEHP exposure increased the contents of total Cytochrome P450s (CYPs) and Cytochrome b5 (Cyt b5) and the activities of NADPH-cytochrome c reductase (NCR) and aniline-4-hydeoxylase (AH) in quail cerebellum. The expression of nuclear xenobiotic receptors (NXRs) and the transcriptions of CYP enzyme isoforms were also influenced in cerebellum by DEHP exposure. These results suggested that DEHP exposure caused the toxic effects of quail cerebellum. DEHP exposure disrupted the cerebellar CYP enzyme system homeostasis via affecting the transcription of CYP enzyme isoforms. The cerebellar P450arom and CYP3A4 might be biomarkers in evaluating the neurotoxicity of DEHP in bird. Finally, this study provided new evidence that DEHP-induced toxic effect of quail cerebellum was associated with activating the NXRs responses and disrupting the CYP enzyme system homeostasis.
DEHP exposure induced the cerebellar toxicity. DEHP caused CYPs disruption in quail cerebellum. DEHP regulated the CYPs homeostasis by activation of NXRs responses and modulation of the transcription of the CYPs isoforms. The cerebellar P450arom and CYP3A4 might be biomarkers in evaluating the neurotoxicity of DEHP in bird. Display omitted
•DEHP induces the cerebellar injury in quail.•DEHP triggers the AhR/PXR/CAR pathway responses in cerebellum.•DEHP disrupts the cerebellar cytochrome P450 enzyme system homeostasis.•Cerebellar P450arom and CYP3A4 might be biomarkers of the DEHP neurotoxicity.
Four unusual indole-terpenoids, penerpenes A–D (1–4), along with two known ones paxilline (5) and emindole SB (6), were isolated from the marine-derived fungus Penicillium sp. KFD28. The absolute ...structures of 1–4 were elucidated on the basis of spectroscopic data and ECD spectra analysis along with quantum ECD calculations. Compounds 1 and 2 showed potent inhibitory activity toward protein tyrosine phosphatases (PTP1B and TCPTP). Plausible biosynthetic pathways of compounds 1–4 are proposed.
Di(2-ethylhexyl) phthalate (DEHP) is an omnipresent environmental pollutant with endocrine disrupting properties. As a plasticizer, DEHP can be leach from the plastic to transfer the external ...environment and thus enters the animal food chain, causing serious damage to the animal organs. The heat-shock response (HSR) comprising heat-shock protein (HSPs) and heat-shock transcription factor (HSFs) plays a pivotal role in various toxic stress conditions. For the sake of investigating the effects of DEHP exposure on cardiac toxicity and the regulation of HSR, male quail were fed the diet with 0, 250, 500 and 750 mg/kg DEHP by gavage administration for 45 days. Histopathological changes including cardiomyocyte swelling and muscle fiber dilatation were observed in the hearts exposed to DEHP. During the DEHP treatment, the mRNA expression of HSP60 and HSP70 were universally reduced, while the expression of other HSPs (HSP10, HSP25, HSP27, HSP40, HSP47, HSP90, HSP110) had different degrees of growth. In addition, the levels of HSF1, HSF2, and HSF3 were significantly increased. Given the facts above, DEHP exposure induced the toxic effects of quail heart. DEHP exposure did great harm to HSR via affecting the synthesis of HSFs to mediate the transcription of the HSPs. Ultimately, this study provided new evidence that DEHP-induced cardiotoxicity in quail was related to activation of HSR and playing a protective role.
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•DEHP exposure induced the renal injury in quail.•DEHP-induced cardiotoxicity is associated with the modulation of HSFs and HSPs.•DEHP exposure activated the HSR pathway responses in the heart.
Di (2-ethyl hexyl) phthalate (DEHP) as a plasticizer can leach away from the plastic and hence entrances into the animal food chain which caused serious hazard in organs of animals, but there are few ...studies on DEHP kidney toxicity. The heat-shock response (HSR) consisting of the HSPs and HSFs plays an important role in various toxicity stress conditions. To investigate the influence on kidney toxicity and the modulation of HSR during DEHP exposure, female quail were fed the diet with 0, 250, 500 and 750 mg/kg DEHP by gavage administration for 45 days. The shrinkages of glomeruli and dilation of kidney tubule epithelia cells were observed in the kidney of DEHP-exposed quail. DEHP treatment could significantly decrease the expressions of HSP25, HSP27, HSP47, HSP60, while the expressions of HSP10, HSP40, HSP70, HSP90, HSP110 were upregulated in the kidney. In addition, the expression levels of HSF1 and HSF3 were significantly increased under DEHP. This is the first study to demonstrate quail exposure to DEHP is in fact detrimental to bird kidney. Besides, DEHP could attack HSR by affecting the synthesis of HSFs to mediate the transcription of the HSPs resulting in kidney damage.
Di (2-ethyl hexyl) phthalate (DEHP) exposure induced the toxic effects of kidney and destroyed the pathophysiological integrity of the kidney in quail. Our findings provide evidence that DEHP-induced nephrotoxicity is associated with heat-shock response (HSR). DEHP exposure activated the HSR signaling pathway to prevent the toxicity in the kidney. Display omitted
•DEHP exposure induced the renal injury in quail.•DEHP-induced nephrotoxicity is associated with the modulation of HSFs and HSPs.•DEHP exposure activated the HSR pathway responses in the kidney.
Five new indole-terpenoids named penerpenes E–I (1–5), along with seven known ones (6–12), were isolated from the marine-derived fungus Penicillium sp. KFD28 from a bivalve mollusk, Meretrix lusoria. ...The structures of the new compounds were elucidated from spectroscopic data and ECD spectroscopic analyses. Compound 1 was assigned as an indole-diterpenoid with a unique 6/5/5/6/6/5/5 heptacyclic ring system. Compound 2 represents an indole-diterpenoid with a new carbon skeleton derived from paxilline by the loss of three carbons (C-23/24/25). Compound 3 contains an additional oxygen atom between C-21 and C-22 compared to paxilline to form an unusual 6/5/5/6/6/7 hexacyclic ring system bearing a 1,3-dioxepane ring, which is rarely encountered in natural products. Compounds 1, 2, 4, and 6 showed inhibitory activities against protein tyrosine phosphatase 1B (PTP1B) with IC50 values of 14, 27, 23, and 13 μM, respectively.
Di (2-ethylhexyl) phthalate (DEHP) is a widely distributed pollutant that is of great concern due to its negative health effects. However, whether DEHP exposure causes liver toxicity in birds remains ...unclear. To clarify the potential hepatotoxicity of DEHP, quails were exposed to 0, 250, 500 and 1000 mg/kg BW/day DEHP by gavage treatment for 45 days. The livers of DEHP-exposed quails showed histomorphological changes. DEHP exposure induced a significant increase in cytochrome P450 enzyme system (CYP450s) activity (including aniline-4-hydroxylase (AH), aminopyrine N-demethylase (APND), erythromycin N-demethylase (ERND) and NADPH-cytochrome C reductase (NCR)) and in the contents of total cytochrome P450 (CYP450) and cytochrome b5 (Cyt b5) in quail liver. DEHP exposure also influenced the expression of nuclear xenobiotic receptors (NXRs) and CYP450 isoforms in the liver. The results suggested that DEHP-induced hepatotoxicity in quail liver is associated with activation of the NXRs pathway responses and disruption of CYP450s homeostasis. This study will help to further elucidate DEHP exposure-induced liver toxicity in quails.
DEHP exposure induced hepatic toxicity. DEHP disrupted hepatic CYP450s homeostasis via affecting the transcription of CYPs. DEHP-induced toxicity was associated with activating AHR/PXR/CAR pathway responses and disrupting the CYP450s homeostasis. Display omitted
•DEHP exposure induces the hepatotoxicity in quail.•DEHP triggers the hepatic AHR/PXR/CAR pathway response.•DEHP disrupts the hepatic CYP450 homeostasis.•DEHP modulates the CYPs isoforms transcription via activating the NXRs pathway.
Microwave discharge electrodeless ultraviolet (MWUV) lamp is a novel type of ultraviolet equipment that utilizes microwave excited plasma to emit ultraviolet light. It offers the advantages of stable ...light intensity and an extended lifespan. Currently, MWUV has been extensively investigated for pollutant degradation, adsorbent regeneration, and bacterial inactivation. Research has demonstrated that MWUV exhibits remarkable efficacy in degrading norfloxacin, ciprofloxacin, dimethoate, etc … Moreover, it enables adsorbent regeneration through microwave thermal release and stimulates electrodeless lamps to generate ultraviolet light, thereby reducing environmental pollution. By utilizing the non-thermal effect of microwaves on bacteria which disrupts their structure, MWUV enhances bacterial inactivation via ultraviolet light exposure. The MWUV can be integrated with various processes, such as photocatalytic systems, photo-Fenton, or photoelectric-Fenton systems, through different configurations including microwave oven reactor, exogenous microwave supply reactor, closed chamber reactor, and complete ultraviolet reactor. These systems have been found to produce abundant reactive oxygen species like ·OH, ·O, and ·OH2. The presence of microwaves promotes free radicals production while lowering the activation energy required for contaminants degradation. Notably, even without microwaves present in the MWUV system, MWUV still exhibit superior photocatalytic performance compared to low-pressure mercury lamps for pollutant degradation. This review provides a detailed introduction to the luminescence mechanisms and structures of MWUV reactors for producing ultraviolet light, as well as their current applications.
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•MWUV lamp generates plasma to emit ultraviolet light by microwave excitation.•A variety of MWUV reactors are constructed in collaboration with various oxidation processes.•The participation of microwave promotes the production of more reactive oxygen species.•MWUV enhances the regeneration effect of adsorbent and inactivation effect of bacterial.
