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In this paper, we study the back-flow problem of boundary layers in two-dimensional unsteady incompressible heat conducting flow. For a kind of monotonic initial and incoming flow, we prove that the first critical point of the tangential velocity profile with respect to the normal variable, if exists, must appear on the boundary if the pressure gradient and temperature in the data are suitable. This critical point is the back-flow point. Moreover, we give a condition on the growth rate of the initial tangential velocity such that there is a back-flow point in the boundary layer. [ABSTRACT FROM AUTHOR]

In this paper, we study the well‐posedness of the thermal boundary layer equation in two‐dimensional incompressible heat conducting flow. The thermal boundary layer equation describes the behavior of thermal layer and viscous layer for the two‐dimensional incompressible viscous flow with heat conduction in the small viscosity and heat conductivity limit. When the initial datum are analytic, with respect to the tangential variable of the boundary, and without the monotonicity condition of the tangential velocity, by using the Littlewood‐Paley theory, we obtain the local‐in‐time existence and uniqueness of solution to this thermal boundary layer problem. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Atrazine (ATR) is a commercially available herbicide that is used worldwide. The intensive use of ATR poses potential risks to animals' and humans' health. Lycopene (LYC) is an anti-oxidative phytochemical that normalizes health hazards triggered by environmental factors. In this study, we aimed to investigate the toxic effects of ATR on the hippocampus and its amelioration by LYC. Male mice were exposed to ATR (50 mg/kg/day or 200 mg/kg/d) and/or LYC (5 mg/kg/d) for 21 days. The results showed that ATR exposure induced hippocampus-dependent learning and memory impairments. ATR-induced ferroptosis in hippocampal cells affects the homeostasis of lipid metabolism, whereas LYC ameliorates the neurotoxic effects of ATR in the hippocampus. LYC inhibited ATR-induced ferroptosis by increasing the expression of HO-1, Nrf2 and SLC7A11. Therefore, this study established that LYC ameliorates ATR-induced spatial learning and memory impairments by inhibiting ferroptosis in the hippocampus and also provides a novel approach for the treatment in contradiction of environmental pollutants. ATR is a kind of herbicide that spreads throughout the environment. Because of its biological activity, particularly antioxidant properties, LYC has attracted a lot of interest. According to our findings, LYC ameliorates ATR-induced spatial learning and memory impairments by inhibiting ferroptosis in the hippocampus of mice. This research may lead to a plausible molecular mechanism for LYC therapy of ATR-induced neurological damage. [Display omitted] • ATR caused spatial learning and memory impairments. • ATR induced ferroptosis in the hippocampus. • LYC can prevent ferroptosis and promote nerve cell repair. • LYC mitigated ATR-induced spatial learning and memory impairments. [ABSTRACT FROM AUTHOR]

To determine dietary selenium (Se) status regulates the transcriptions of selenoproteome and activities of selenoenzymes in chicken kidney, 1-day-old chickens received low Se (0.028 mg Se per kg of diet) or super-nutritional Se (3.0 or 5.0 mg Se per kg of diet) in their diets for 8 weeks. It was observed that dietary low or super-nutritional Se did not make renal appearance pathological changes in chicken. Low Se significantly reduced total antioxidant capability (T-AOC), glutathione (GSH) content, but malondialdehyde (MDA) content in the kidney increased and decreased glutathione peroxidase (Gpx) and thioredoxin reductase (TrxR) activity with changes in their mRNA levels. Super-nutritional Se (3.0 mg/kg) increased T-AOC and GSH contents then made them reduce, but it reduced MDA content significantly, elevated then reduced Gpx activity, and decreased TrxR activity with changes in their mRNA levels. Dietary low Se downregulated the mRNA expressions of Gpx1-4, Txnrd3, Sepn1, Selw, Sepx1, Selh, and SEPSECS. At super-nutritional Se, most selenoproteins were upregulated in chicken kidney, but Sepp2 and Sep15 was only upregulated in Se excess (5.0 mg/kg) bird. These results indicated that dietary Se status stabilizes normal renal physiology function via regulation of the selenoprotemic transcriptions and selenoenzyme activities in avian. [ABSTRACT FROM AUTHOR]

There has been a gradual increase in production and consumption of atrazine (ATR) in agriculture to meet the population rising demands. Female reproduction is necessary for growth and maintenance of population. However, ATR impact on females and particularly ovarian developmental toxicity is less clear. The aim of this study was to define the pathways by which ATR exerted toxic effects on ovarian development of ovary and hypothalamo-pituitary-ovarian (HPO) axis. Female quails were dosed by oral gavage from sexual immaturity to maturity with 0, 50, 250 and 500 mg ATR/kg/d for 45 days. ATR had no effect on mortality but depressed feed intake and growth and influenced the biochemical parameters. Notably, the arrested development of ovaries and oviducts were observed in ATR-exposed quails. The circulating concentrations of E2, P, LH and PRL were unregulated and FSH and T was downregulated in ATR-treated quails. The mRNA expression of GnRH in hypothalamo and LH in pituitary and FSH in ovary was downregulated significantly by ATR exposure and FSH and PRL in pituitary were upregulated. ATR exposure upregulated the level of P450scc, P450arom, 3β-HSD and 17β-HSD in ovary and downregulated ERβ expression in female quails. However, ATR did not change ERα expression in ovary. This study provides new insights regarding female productive toxicology of ATR exposure. Ovary and oviduct in sexually maturing females were target organs of ATR-induced developmental toxicity. We propose that ATR-induced developmental abnormality of ovary and oviduct is associated with disruption of gonadal hormone balance and HPO axis in female quails. [ABSTRACT FROM AUTHOR]

Di(2-ethylhexyl) phthalate (DEHP) is an omnipresent environmental pollutant. It has been determined that DEHP is involved in multiple health disorders. Lycopene (Lyc) is a natural carotenoid pigment, with anti-inflammatory and antioxidant properties. However, it is not clear whether Lyc can protect the spleen from DEHP-induced oxidative damage. A total of 140 mice were randomly divided into seven groups (n = 20) and continuously gavaged with corn oil, distilled water, DEHP (500 or 1000 mg/kg BW/day) and/or Lyc (5 mg/kg BW/day) for 28 days. Histopathological and ultrastructural results showed a DEHP-induced inflammatory response and mitochondrial injuries. Moreover, DEHP exposure induced redox imbalance, which resulted in the up-regulation of ROS activity and MDA content, and the down-regulation of T-AOC, T-SOD and CAT in the DEHP groups. Simultaneously, our results also demonstrated that DEHP-induced kelch-like ECH-associated protein 1 (Keap1) expression was downregulated, and the expression levels of P62, nuclear factor erythroid 2-related factor (NRF2) and their downstream target genes were up-regulated. However, the supplementary Lyc reverted these changes to normal levels. Together, Lyc prevented DEHP-induced splenic injuries by regulating the P62-Keap1-NRF2 signaling pathway. Hence, the protective effects of Lyc might be a therapeutic strategy to ameliorate DEHP-induced splenic damage. Exposure to persistent environmental pollutants such as di(2-ethylhexyl) phthalate (DEHP) has been involved in multiple health disorders, including splenic diseases. In this study, we clarified the potential protective effect of lycopene on DEHP-induced splenic injury. The results showed that Lyc inhibited DEHP induced oxidative damage by regulating the P62-Keap1-NRF2 signaling pathway, indicating that Lyc could alleviate the toxic effects of DEHP and may be helpful in reducing spleen injury. [Display omitted] • Lyc alleviated DEHP exposure-induced splenic injury. • Lyc alleviated the DEHP exposure-induced redox imbalance. • Lyc mitigated the inhibition of P62-Keap1-NRF2 pathway induced by DEHP exposure. • Lyc alleviated the splenic cell mitochondrial injuries induced by DEHP exposure. [ABSTRACT FROM AUTHOR]

Di (2-ethylhexyl) phthalate (DEHP) is a widespread plasticizer that persists in the environment and can significantly contribute to serious health hazards of liver especially oxidative stress injury. Lycopene (LYC) as a carotenoid has recently gained widespread attention because of antioxidant activity. However, the potential mechanism of DEHP-induced hepatotoxicity and antagonism effect of LYC on it are still unclear. To explore the underlying mechanisms of this hypothesis, the mice were given by gavage with LYC (5 mg/kg) and DEHP (500 or 1000 mg/kg). The data suggested that DEHP caused liver enlargement, reduction of antioxidant activity markers, increase of oxidative stress indicators and disorder of cytochrome P450 enzymes system (CYP450s) homeostasis. DEHP-induced reactive oxygen species (ROS) activated the NF-E2-relatedfactor2 (Nrf2) and nuclear xenobiotic receptors (NXRs) system including Aryl hydrocarbon receptor (AHR), Pregnane X receptor (PXR) and Constitutive androstane receptor (CAR). Interestingly, these disorders and injuries were prevented after LYC treatment. Taken together, DEHP administration resulted in hepatotoxicity including oxidative stress injury and disordered CYP450 system, but these alterations might be ameliorated by LYC via crosstalk between AHR–Nrf2 pathway. This study suggested that DEHP could result hepatotoxicity including oxidative stress injury and disorder of CYP450 system, but these alterations could be ameliorated by LYC via crosstalk between AHR–Nrf2 pathway. [Display omitted] • DEHP induced hepatic oxidative stress damage. • DEHP caused hepatic CYP450s imbalance. • LYC prevented CYP450s homeostasis disorders by nuclear receptor system. • LYC ameliorated oxidative stress damage via crosstalk between AHR–Nrf2 pathway. [ABSTRACT FROM AUTHOR]

Atrazine (ATR) is a widely used herbicide with biologically toxic effects that can lead to neurotoxicity. Lycopene (LYC) is an antioxidant with chemoprotective properties. However, little know about the mechanisms of preventative interventions about LYC alleviated ATR-induced neurotoxicity. Male mice were treated with distilled water (C), 5 mg/kg BW/day LYC (L), 50 and 200 mg/kg BW/day ATR (A1, A2), respectively and LYC + ATR (A1+L, A2+L). ATR promoted oxidative stress and inflammatory damage, as showed by the effects on MDA, H 2 O 2 , IL-6 and TNF-α accumulation, and IL-10, SOD, CAT and GSH depletion, which caused neuronal swelling and mitochondrial vacuolar degeneration. ATR disrupted the CYP450s balance via increasing contents of CYP450 and cytochrome B5, enhancing activities of NCR and ERND and activating NXRs and NXRs-related transcription factors. However, all these effects were reversed by LYC pretreatment. Collectively, these data indicated that LYC inhibited ATR-induced oxidative damage through modulating xenobiotic-sensing nuclear receptors and CYP450s. [Display omitted] • LYC inhibits ATR exposure-induces neurotoxicity. • LYC alleviates ATR exposure-induces AHR/PXR/CAR pathway responses. • LYC alleviates ATR-induces the CYP450 homeostasis disorders and CYPs transcription. • LYC alleviates ATR exposure triggers oxidative stress and inflammatory response. [ABSTRACT FROM AUTHOR]

An increasing number of epidemiologic studies show that women have a special exposure profile to phthalates, and the exposures have attracted attention regarding their potential health hazards. Here, we developed a model for studying the ovarian action of di-(2-ethylhexyl) phthalate (DEHP) and its major metabolite monoethylhexyl phthalate (MEHP). In vivo, treatment with DEHP (250, 500, and 1000 mg kg^-1) induced decreased thickness of ovarian granulosa cell layer and mitochondrial damage in quail, caused oxidative stress, interfered with the transcription of hypothalamic-pituitary-ovarian axis (HPOA) steroid hormone-related factors (increased transcription of StAR , 3β-HSD , P450scc , and LH and decreased transcription of 17β-HSD , P450arom, FSH , and ERβ), and blocked the secretion of steroid hormones (decreased FSH, E 2 , and T levels and increased LH, P, and PRL levels). In vitro, granulosa cells were cultured with MEHP (50, 100, and 200 μM), activator of PPARγ (rosiglitazone, 50 μM), or antagonist of PPARγ (GW9662, 10 μM) for 24 h and gene and protein expression were analyzed by real time RT-PCR and western blot. Rosiglitazone, like MEHP, significantly decreased mRNA and protein levels of P450arom. Antagonist GW9662 partially blocked the suppression of P450arom by MEHP, suggesting that MEHP acts through PPARγ, but not exclusively. Our model shows that MEHP acts on granulosa cells in quail by stimulating PPARs, which leads to decreased gene and protein expression of P450arom. Therefore, the environmental endocrine disruptor DEHP and its major metabolite MEHP act through a receptor-mediated signaling pathway to inhibit the production of estradiol, interfere with the modulation of HPOA, suppress the synthesis of sex hormones, and cause sex hormone secretion disorders, resulting in severe toxicity in the female reproductive system. A framework for an adverse outcome pathway of DEHP/MEHP-induced ovarian toxicity was constructed, which can facilitate an improved understanding of the mechanism of female reproductive toxicity. The environmental contaminant DEHP and its metabolite MEHP act through a receptor-mediated signaling pathway to suppress estradiol production in the ovary, interfere with the regulation of the hypothalamus-pituitary-ovarian gonadal axis, hinder the synthesis of sex hormones, and trigger sex hormone secretion disorders, leading to serious dose-dependent toxicity of the reproductive system. A framework for an adverse outcome pathway of DEHP/MEHP-induced ovarian toxicity was constructed, which can facilitate an improved understanding of the mechanism of female reproductive toxicity. Unlabelled Image • Exposure to DEHP induced ovarian developmental disorders in quail. • DEHP disrupted sex hormone levels by interfering with the regulation of HPOA. • MEHP decreased aromatase level in the granulosa cell by activating the PPARs. • DEHP and its metabolite MEHP lead to toxicity on the reproductive system. • A framework for an AOP of DEHP/MEHP-induced ovarian toxicity was constructed. [ABSTRACT FROM AUTHOR]