Zearalenone (ZEA), a common contaminant in food and feedstuffs, threatens human and animal health. The present study aimed to investigate the protective effects of modified palygorskite (MPal), a ZEA-targeted adsorbent, on broilers (young chickens) fed a ZEA-contaminated diet. Broilers were subjected to one of three treatments for a period of 42 days: a basal diet (control group), a ZEA- contaminated diet, and a ZEA-contaminated diet supplemented with 1 g/kg of MPal. Blood was collected for serum metabolite assay, and liver and kidney were sampled to determine ZEA residue and antioxidant-related parameters, using commercial spectrophotometric kits. Compared with the basal diet, the ZEA- contaminated diet resulted in compromised growth performance (reduced daily gain and feed intake during finisher period), disordered relative liver weight (decreased at 21 days but increased at 42 days), increased ZEA residue in liver and kidney, abnormal serum metabolites (decreased total protein content but increased alanine aminotransferase activity at 21 and 42 days, reduced albumin content at 21 days, and elevated aspartate aminotransferase activity at 42 days), and disrupted antioxidant capacities of broilers (increased total superoxide dismutase (T-SOD) activity in liver at 21 and 42 days, decreased T-SOD activity in kidney at 21 and 42 days, and in serum at 42 days, greater malondialdehyde accumulation in liver and kidney at 42 days, and lower glutathione content in kidney at 21 days). The adverse consequences resulting from the ZEA-contaminated diet were relieved by the supplementation of MPal (except albumin concentration in serum and T-SOD activity in liver at 21 days), with the values of growth-performance parameters, liver weight, renal ZEA accumulation, total protein content, transaminase activity at 42 days, and antioxidant indexes being similar to those in the control group. These results suggested that MPal supplementation could promote growth performance, attenuate liver damage, and improve the antioxidant abilities of broilers fed ZEA-contaminated diet by reducing ZEA accumulation.

This study is aimed to evaluate the effect and underling mechanism of dietary supplementation with pyrroloquinoline quinone (PQQ) disodium on improving inflammatory liver injury in piglets challenged with lipopolysaccharide (LPS). A total of seventy-two crossbred barrows were allotted into four groups as follows: the CTRL group (basal diet + saline injection); the PQQ group (3 mg/kg PQQ diet + saline injection); the CTRL + LPS group (basal diet + LPS injection) and the PQQ + LPS group (3 mg/kg PQQ diet + LPS injection). On days 7, 11 and 14, piglets were challenged with LPS or saline. Blood was sampled at 4 h after the last LPS injection (day 14), and then the piglets were slaughtered and liver tissue was harvested. The results showed that the hepatic morphology was improved in the PQQ + LPS group compared with the CTRL + LPS group. PQQ supplementation decreased the level of serum inflammatory factors, aspartate aminotransferase and alanine transaminase, and increased the HDL-cholesterol concentration in piglets challenged with LPS; piglets in the PQQ + LPS group had lower liver mRNA level of inflammatory factors and protein level of α-smooth muscle actin than in the CTRL + LPS group. Besides, mRNA expression of STAT3/TGF-β1 pathway and protein level of p-STAT3(Tyr 705) were decreased, and mRNA level of PPARα and protein expression of p-AMPK in liver were increased in the PQQ + LPS group compared with the CTRL + LPS group (P < 0·05). In conclusion, dietary supplementation with PQQ alleviated inflammatory liver injury might partly via inhibition of the STAT3/TGF-β1 pathway in piglets challenged with LPS.

Methotrexate (MTX) is a cytotoxic immunosuppressant that is widely used in the treatment of tumours, rheumatoid arthritis and psoriasis. This study aims to evaluate the effects of whey proteins on MTX-induced liver and kidney damage by focusing on oxidant–antioxidant systems and eating habits. The study was conducted in four groups of thirty Sprague–Dawley rats (control, control + whey protein concentrate (WPC), MTX, MTX + WPC). A single dose of 20 mg/kg MTX was administered intraperitoneally to the MTX groups. Control and MTX groups were given 2 g/kg WPC by oral gavage every day for 10 d. At the end of day 10, blood samples were drawn and liver and kidney tissues were removed. MTX administration increased the lipid peroxidation level and decreased glutathione level, superoxide dismutase and glutathione-S-transferase activities in the liver and kidney. Administration of WPC significantly reduced the damage caused by MTX in the liver and kidney. While a decrease in serum urea level and an increase in serum creatinine level were detected in the MTX group, WPC administration reversed these results up to control group levels. Administration of WPC to the MTX group significantly reversed the histopathological damage scores of the liver and kidney. WPC administration ameliorated the MTX-induced oxidative damage in the liver and kidney tissues due to its antioxidant properties. Liver and kidney damage can be prevented by using whey proteins as a nutraceutical in MTX therapy. In conclusion, whey proteins demonstrated a protective effect against MTX-induced liver and kidney damage.

In recent years, a possible defect in vitamin A metabolism in recessive white canaries (Serinus canaria,) has been repeatedly discussed. It has widely been accepted that a reduced absorption of carotenoids from the small intestine results in an insufficient synthesis of vitamin A. Moreover, the uptake of vitamin A from the lower intestine has also been discussed.

The aim of the present study was to investigate the utilization of ß-carotene and vitamin A by recessive white canaries (in comparison to coloured ones) as well as to quantify the accretion of vitamin A in the liver and vitamin A levels in plasma and fat tissues of canaries fed different doses of ß-carotene (≍ 6000iu vitamin A kg−1 diet) vs vitamin A (6000 or 18 000iu kg−1 diet).

The results were as follows:

• i) coloured canaries supplied exclusively with ß-carotene maintained normal vitamin A levels in the liver. These data indicated that conversion rates of ß-carotene to vitamin A (as established for poultry) were appropriate;

• ii) recessive white canaries were totally unable to utilize ß-carotene (based on vitamin A levels in blood, liver and fat);

• iii) in comparison to coloured canaries, their efficiency in utilizing retinol was significantly lower. They needed three times the vitamin A intake of coloured canaries to achieve the same vitamin A levels in the liver;

• iv) plasma vitamin A levels in coloured canaries did not reflect the vitamin A supply, but this blood level could be used to determine vitamin A status in recessive white birds.

Recommendations of vitamin A supplements for recessive white canaries should be given based on these data.

Many epidemiological studies have emphasised the relation between carotenoid dietary intake and their circulating concentrations and beneficial health effects, such as lower risk of cardiometabolic diseases and cancer. However, there is dispute as to whether the attributed health benefits are due to native carotenoids or whether they are instead induced by their metabolites. Several categories of metabolites have been reported, most notably involving (a) modifications at the cyclohexenyl ring or the polyene chain, such as epoxides and geometric isomers, (b) excentric cleavage metabolites with alcohol-, aldehyde- or carboxylic acid-functional groups or (c) centric cleaved metabolites with additional hydroxyl, aldehyde or carboxyl functionalities, not counting their potential phase-II glucuronidated / sulphated derivatives. Of special interest are the apo-carotenoids, which originate in the intestine and other tissues from carotenoid cleavage by β-carotene oxygenases 1/2 in a symmetrical / non-symmetrical fashion. These are more water soluble and more electrophilic and, therefore, putative candidates for interactions with transcription factors such as NF-kB and Nrf2, as well as ligands for RAR–RXR nuclear receptor interactions. In this review, we discuss in vivo detected apo-carotenoids, their reported tissue concentrations, and potential associated health effects, focusing exclusively on the human situation and based on quantified / semi-quantified carotenoid metabolites proven to be present in humans.

An isotope dilution model for partitioning phenylalanine and tyrosine uptake by the liver of the lactating dairy cow is constructed and solved in the steady state. An original ten-pool model is adopted and solved by cleaving it into two five-pool sub-models, one representing phenylalanine and the other tyrosine. If assumptions are made, model solution permits calculation of the rate of phenylalanine and tyrosine uptake from portal vein and hepatic arterial blood supply, hydroxylation, and synthesis and degradation of constitutive protein. The model requires the measurement of plasma flow rate through the liver in combination with amino acid concentrations and plateau isotopic enrichments in arterial and portal and hepatic vein plasma during a constant infusion of [1-13C]phenylalanine and [2,3,5,6-2H]tyrosine tracers. It also requires estimates of the rate of oxidation and protein export secretion. Analysis of measurement errors in experimental enrichments and infusion rates on model solutions indicated that accurate values of the intracellular and extracellular enrichments are central to minimising errors in the calculated flows. Solving the model by cleaving into two five-pool schemes rather than solving the ten-pool scheme directly is preferred as there appears to be less compounding of errors and the results consistently appear to be more biologically feasible. The model provides a means for assessing the impact of hepatic metabolism on amino acid availability to peripheral tissues such as the mammary gland.

This perspective article applies public health principles to improve the physical health of selected populations with mental disorders. Two preventable adverse outcomes, poorer physical health and premature mortality, are described across mental disorders. Evidence of the lifetime effects of adverse childhood experiences and inequalities is presented: these are the ‘causes of the causes’. Seven drivers of physical disorders are illustrated that drive preventable deaths and as doctors, psychiatrists must lead from the front to reverse rising mortality. Evidence supports universal and selective interventions and even the most difficult challenges such as weight gain and opioid misuse are an opportunity for psychiatry to engage with individual patients and their organisations, public health colleagues, health systems and beyond. Interventions complement and do not replace existing clinical practices that reduce self-harm and prevent suicide. Mental health teams already do most of the work in this arena, and the case is made to refocus on physical health with task sharing. The top 10 recommendations within a personalised medicine framework are listed in this paper as a starting point.

Vitamin E (α-tocopherol; VE) is known to be regenerated from VE radicals by vitamin C (L-ascorbic acid; VC) in vitro. However, their in vivo interaction in various tissues is still unclear. Therefore, we alternatively examined the in vivo interaction of VC and VE by measurement of their concentrations in various tissues of senescence marker protein-30 (SMP30) knockout (KO) mice as a VC synthesis deficiency model. Male SMP30-KO mice were divided into four groups (VC+/VE+, VC+/VE–, VC–/VE+ and VC–/VE–), fed diets with or without 500 mg/kg VE and given water with or without 1·5 g/l VC ad libitum. Then, VC and VE concentrations in the plasma and various tissues were determined. Further, gene expression levels of transporters associated with VC and VE, such as α-tocopherol transfer protein (α-TTP) and sodium-dependent vitamin C transporters (SVCTs), were examined. These results showed that the VE levels in the VC-depleted (VC–/VE+) group were significantly lower than those in the VC+/VE+ group in the liver and heart; the VC levels in the VE-depleted (VC+/VE–) group were significantly lower than those in the VC+/VE+ group in the kidneys. The α-TTP gene expression in the liver and kidneys was decreased by VC and/or VE depletion. Moreover, SVCT1 gene expression in the liver was decreased by both VC and VE depletion. In conclusion, these results indicate that VC spares VE mainly in the liver and heart and that VE spares VC in the kidneys of SMP30-KO mice. Thus, interaction between VC and VE is likely to be tissue specific.

Despite the apparent beneficial effects of probiotics/synbiotics on glucose haemostasis, lipid profile and inflammatory responses, it is not clear whether these beneficial effects also impact renal and hepatic function in diabetes. Therefore, we sought to assess the effect of probiotics/synbiotics supplementation on renal and liver biomarkers in adults with type 2 diabetes mellitus (T2DM) using a systematic review and meta-analysis of randomised controlled trials (RCT). PubMed, Scopus, Web of Science and Cochrane Library were systematically searched, up to February 2021. The pooled weighted mean difference (WMD) was estimated using a random-effects model. The methodological quality of studies, as well as certainty of evidence, was assessed using standard scales. Fifteen related trials were identified. Meta-analysis of six trials, involving 426 participants, indicated that probiotics/synbiotics supplementation reduced serum levels of creatinine (WMD = −0·10 mg/dl, 95 % CI −0·20, −0·00; P = 0·01; I 2 = 87·7 %; P-heterogeneity < 0·001), without any significant effect on blood urea nitrogen (BUN), glomerular filtration rate or microalbuminuria. No significant improvement was found on liver biomarkers following probiotics/synbiotics supplementation. The subgroup analysis showed a significant improvement in BUN when follow-up duration lasted for 12 weeks or more (WMD = −1·215 mg/dl, 95 % CI −1·933, −0·496; P = 0·001) and in creatinine levels in patients with renal dysfunction (WMD = −0·209 mg/dl, 95 % CI −0·322, −0·096; P < 0·001). Our results are insufficient to advocate the use of probiotics/synbiotics for improving renal or liver function in patients with T2DM. Indeed, due to the low certainty of evidence, these findings need to be affirmed in further high-quality RCT.

In this work, we investigated the labeling efficiency of hydrophilic (DAPI) and hydrophobic (Nile Red) fluorescent probes using uni- and bi-directional diffusion on porcine liver tissue sections on the order of a few hundred microns in thickness. Bi-directional diffusion significantly enhanced the penetration of probes. Although diffusion most accurately describes the labeling process, we found that after removal of the labeling molecules residual probe molecules in the tissue sections continued to be transported deeper into the tissue resulting in additional tissue constituents being labeled. Our study shows that bi-directional labeling can significantly enhance the labeling of thick tissues for applications in which structural information in three dimensions is needed.

Ascaris lumbricoides and Ascaris suum are helminth parasites of humans and pigs, respectively. The life cycle of Ascaris sets it apart from the other soil-transmitted helminths because of its hepato-tracheal migration. Larval migration contributes to underestimated morbidity in humans and pigs. This migration, coupled with a lack of a murine model in which the Ascaris parasite might complete its life cycle, has undoubtedly contributed to the neglected status of the ascarid. Our knowledge of the epidemiology of adult worm infections had led us to an enhanced understanding of patterns of infection such as aggregation and predisposition; however, the mechanisms underlying these complex phenomena remain elusive. Carefully controlled experiments in defined inbred strains of mice – with enhanced recovery of larvae in tandem with measurements of cellular, histopathological and molecular processes – have greatly enhanced our knowledge of the early phase of infection, a phase crucial to the success or failure of adult worm establishment. Furthermore, the recent development of a mouse model of susceptibility and resistance, with highly consistent and diverging Ascaris larval burdens in the murine lungs, represents the extremes of the host phenotype displayed in the aggregated distribution of worms and provides an opportunity to explore the mechanistic basis that confers predisposition to light and heavy Ascaris infection. Certainly, detailed knowledge of the cellular hepatic and pulmonary responses at the molecular level can be accrued from murine models of infection and, once available, may enhance our ability to develop immunomodulatory therapies to elicit resistance to infection.

The objective of this study was to compare the effect of two different preventive protocols, on serum β-hydroxybutyrate (BHB) concentration and liver health indices pre-partum and during early-lactation in high-yielding Holstein dairy cows. One hundred cows were randomly divided into three groups: control group (CTRL, n = 20, without preventive treatment), second group (SUPP, n = 40 animals treated with a compound based on acetyl-methionine, inositol, cyanocobalamin, l-alanine, l-arginine, l-threonine, l-glutamic acid supplementation and α-lipoic acid) and third group (MON, n = 40 animals treated with monensin). Blood samples were collected from all cows at on 3 occasions pre-partum and 3 occasions post-partum. Body condition (BCS) score was evaluated and glucose, non-esterified fatty acids (NEFA), BHB, triglycerides, total cholesterol, alanine aminotransferase (ALT), aspartate aminotransferase (AST), γ-glutamyltransferase (GGT), total bilirubin, total proteins, globulins, albumin and urea concentrations were assessed. Two-way repeated measures analysis of variance was applied. Statistically significant differences among the three experimental groups were found in the values of all studied parameters (P < 0.05). Our results confirm the established beneficial effect of MON treatment in decreasing BHB levels and increasing glucose availability after calving. Serum biochemical analysis revealed the expected post-partum alterations attributable to adaptations that influenced the metabolism and liver function in CTRL, whereas these alterations were reduced or absent in SUPP and MON. Results from the present study suggest that both preventive protocols, but in particular SUPP, could positively affect selected indicators of energy metabolism reducing the risk of hyperketonaemia and increase of liver function in Holstein dairy cows, both pre- and post-partum.

The soil-transmitted helminth Ascaris lumbricoides infects ~800 million people worldwide. Some people are heavily infected, harbouring many worms, whereas others are only lightly infected. The mechanisms behind this difference are unknown. We used a mouse model of hepatic resistance to Ascaris, with C57BL/6J mice as a model for heavy infection and CBA/Ca mice as a model for light infection. The mice were infected with the porcine ascarid, Ascaris suum or the human ascarid, A. lumbricoides and immune cells in their livers and spleens were enumerated using flow cytometry. Compared to uninfected C57BL/6J mice, uninfected CBA/Ca mice had higher splenic CD4+ and γδ T cell counts and lower hepatic eosinophil, Kupffer cell and B cell counts. Infection with A. suum led to expansions of eosinophils, Kupffer cells, monocytes and dendritic cells in the livers of both mouse strains and depletions of hepatic natural killer (NK) cells in CBA/Ca mice only. Infection with A. lumbricoides led to expansions of hepatic eosinophils, monocytes and dendritic cells and depletions of CD8+, αβ, NK and NK T cells in CBA/Ca mice, but not in C57BL/6J mice where only monocytes expanded. Thus, susceptibility and resistance to Ascaris infection are governed, in part, by the hepatic immune system.

Although abundant evidence exists that adverse events during pregnancy lead to chronic conditions, there is limited information on the impact of acute insults such as sepsis. This study tested the hypothesis that impaired fetal development leads to altered organ responses to a septic insult in both male and female adult offspring. Fetal growth restricted (FGR) rats were generated using a maternal protein-restricted diet. Male and female FGR and control diet rats were housed until 150–160 d of age when they were exposed either a saline (control) or a fecal slurry intraperitoneal (Sepsis) injection. After 6 h, livers and lungs were analyzed for inflammation and, additionally, the amounts and function of pulmonary surfactant were measured. The results showed increases in the steady-state mRNA levels of inflammatory cytokines in the liver in response to the septic insult in both males and females; these responses were not different between FGR and control diet groups. In the lungs, cytokines were not detectable in any of the experimental groups. A significant decrease in the relative amount of surfactant was observed in male FGR offspring, but this was not observed in control males or in female animals. Overall, it is concluded that FGR induced by maternal protein restriction does not impact liver and lung inflammatory response to sepsis in either male or female adult rats. An altered septic response in male FGR offspring with respect to surfactant may imply a contribution to lung dysfunction.

Deep-fried vegetable oils are reused multiple times to save costs, and their chronic consumption may cause organ dysfunction. In this study, we assessed the modulatory effects of lipid-solubles from ginger and turmeric that may migrate to oils during heating, on the cardio-hepatic antioxidant defence response and blood pressure in rats. Male Wistar rats were fed with: (1) control (native rapeseed (N-CNO) or native sunflower (N-SFO)) oil, (2) heated (heated rapeseed (H-CNO) or heated sunflower (H-SFO)) oil and (3) heated oil with ginger or turmeric (heated rapeseed oil with ginger (H-CNO + GI) or heated rapeseed oil with turmeric (H-CNO + TU), heated sunflower oil with ginger (H-SFO + GI) or heated sunflower oil with turmeric (H-SFO + TU)) for 120 d. Oxidative stress (OS) markers, antioxidant enzymes, nitric oxide synthase-2 (NOS-2), intercellular adhesion molecule-1 (ICAM-1), nuclear factor erythroid 2-related factor 2 (NRF-2), markers of hepatic and cardiac function and blood pressure were assessed. Feeding heated oils (H-CNO or H-SFO) (1) increased OS markers, NOS-2 and ICAM-1 expression; (2) decreased antioxidant enzyme activity and NRF-2 level; (3) increased marker enzymes of hepatic and cardiac function and (4) increased systolic and diastolic blood pressure significantly (P < 0·05), when compared with respective native oils (N-CNO or N-SFO). However, feeding oils heated with ginger or turmeric positively countered the changes induced by heated oils. Consumption of repeatedly heated oil causes cardio-hepatic dysfunction by inducing OS through NRF-2 down-regulation. Lipid-solubles from ginger and turmeric that may migrate to oil during heating prevent the oxidative stress and blood pressure triggered by heated oils in rats.