Gut microbiota contributes to bisphenol A-induced maternal intestinal and placental apoptosis, oxidative stress, and fetal growth restriction in pregnant ewe model by regulating gut-placental axis.

BACKGROUND: Bisphenol A (BPA) is an environmental contaminant with endocrine-disrupting properties that induce fetal growth restriction (FGR). Previous studies on pregnant ewes revealed that BPA exposure causes placental apoptosis and oxidative stress (OS) and decreases placental efficiency, consequently leading to FGR. Nonetheless, the response of gut microbiota to BPA exposure and its role in aggravating BPA-mediated apoptosis, autophagy, mitochondrial dysfunction, endoplasmic reticulum stress (ERS), and OS of the maternal placenta and intestine are unclear in an ovine model of gestation. RESULTS: Two pregnant ewe groups (n = 8/group) were given either a subcutaneous (sc) injection of corn oil (CON group) or BPA (5 mg/kg/day) dissolved in corn oil (BPA group) once daily, from day 40 to day 110 of gestation. The maternal colonic digesta and the ileum and placental tissue samples were collected to measure the biomarkers of autophagy, apoptosis, mitochondrial dysfunction, ERS, and OS. To investigate the link between gut microbiota and the BPA-induced FGR in pregnant ewes, gut microbiota transplantation (GMT) was conducted in two pregnant mice groups (n = 10/group) from day 0 to day 18 of gestation after removing their intestinal microbiota by antibiotics. The results indicated that BPA aggravates apoptosis, ERS and autophagy, mitochondrial function injury of the placenta and ileum, and gut microbiota dysbiosis in pregnant ewes. GMT indicated that BPA-induced ERS, autophagy, and apoptosis in the ileum and placenta are attributed to gut microbiota dysbiosis resulting from BPA exposure. CONCLUSIONS: Our findings indicate the underlying role of gut microbiota dysbiosis and gut-placental axis behind the BPA-mediated maternal intestinal and placental apoptosis, OS, and FGR. The findings further provide novel insights into modulating the balance of gut microbiota through medication or probiotics, functioning via the gut-placental axis, to alleviate gut-derived placental impairment or FGR. Video Abstract.

Low levels of Cd2+ combined with procymidone may cause ovarian damage in mice via unfolded protein response.

As no study about the combined effect of low levels of Cd2+ with procymidone (PCM) on organs and organisms, we investigated their actions on mouse-ovary in vivo and in vitro. Four-week mice were treated with corn oil for the control group, corn oil + 0.0045 mg/L Cd2+ (CdCl2 was dissolved in ultrapure water and freely consumed by mice) for Cd2+ group, 50 mg/kg/d PCM (suspended in corn oil and administered orally to mice) for PCM group, and 50 mg/kg/d PCM + 0.0015 (0.0045 and 0.0135) mg/L Cd2+ for L+ (M+ and H+) PCM group for 21 days. For in vitro experiment, the cultured ovaries were treated with acetone for the control group, 0.1% acetone + 8.4 µg/L Cd2+ for the Cd2+ group, 0.63 mg/L PCM (dissolved in acetone) for the PCM-group, and 0.63 mg/L PCM + 2.8 (8.4 and 25.2) µg/L Cd2+ for L+ (M+ and H+) PCM group for 7 days. Mouse body weight in each treatment group, the weight and volume of ovaries in all PCM groups were lower than the control. Both in vivo and in vitro, all-stage follicle numbers were lower in M+PCM and H+PCM groups, whereas the atretic follicles and CASPASE3/8 were higher; meanwhile, lower estradiol and progesterone and higher unfolded protein response (UPR) members in all PCM groups. L+, M+, and H+PCM groups had further ovarian damage and stronger UPR than PCM groups, as did M+PCM groups over Cd2+ groups. It is hypothesized low-level PCM and Cd2+ may mutually promote each other's triggered UPR and exacerbate ovarian damage.

Multilocus functional characterization of indigenous and exotic inbreds for dgat1-2, fatb, ge2 and wri1a genes affecting kernel oil and fatty acid profile in maize.

Demand for maize oil is progressively increasing due to its diverse industrial applications, aside from its primary role in human nutrition and animal feed. Oil content and composition are two crucial determinants of maize oil in the international market. As kernel oil in maize is a complex quantitative trait, improving this trait presents a challenge for plant breeders and biotechnologists. Here, we characterized a set of 292 diverse maize inbreds of both indigenous and exotic origin by exploiting functional polymorphism of the dgat1-2, fatb, ge2, and wri1a genes governing kernel oil in maize. Genotyping using gene-based functional markers revealed a lower frequencies of dgat1-2 (0.15) and fatb (0.12) mutant alleles and a higher frequencies of wild-type alleles (Dgat1-2: 0.85; fatB: 0.88). The favorable wri1a allele was conserved across genotypes, while its wild-type allele (WRI1a) was not detected. In contrast, none of the genotypes possessed the ge2 favorable allele. The frequency of favorable alleles of both dgat1-2 and fatb decreased to 0.03 when considered together. Furthermore, pairwise protein-protein interactions among target gene products were conducted to understand the effect of one protein on another and their responses to kernel oil through functional enrichments. Thus, the identified maize genotypes with dgat1-2, fatb, and wri1a favourable alleles, along with insights gained through the protein-protein association network, serve as prominent and unique genetic resources for high-oil maize breeding programs. This is the first comprehensive report on the functional characterization of diverse genotypes at the molecular and protein levels.

Blockade of C5aR1 alleviates liver inflammation and fibrosis in a mouse model of NASH by regulating TLR4 signaling and macrophage polarization.

BACKGROUND: Nonalcoholic steatohepatitis (NASH) is an advanced form of chronic fatty liver disease, which is a driver of hepatocellular carcinoma. However, the roles of the C5aR1 in the NASH remain poorly understood. Here, we aimed to investigate the functions and mechanisms of the C5aR1 on hepatic inflammation and fibrosis in murine NASH model. METHODS: Mice were fed a normal chow diet with corn oil (ND + Oil), a Western diet with corn oil (WD + Oil) or a Western diet with carbon tetrachloride (WD + CCl4) for 12 weeks. The effects of the C5a-C5aR1 axis on the progression of NASH were analyzed and the underlying mechanisms were explored. RESULTS: Complement factor C5a was elevated in NASH mice. C5 deficiency reduced hepatic lipid droplet accumulation in the NASH mice. The hepatic expression levels of TNFα, IL-1ß and F4/80 were decreased in C5-deficient mice. C5 loss alleviated hepatic fibrosis and downregulated the expression levels of α-SMA and TGFß1. C5aR1 deletion reduced inflammation and fibrosis in NASH mice. Transcriptional profiling of liver tissues and KEGG pathway analysis revealed that several pathways such as Toll-like receptor signaling, NFκB signaling, TNF signaling, and NOD-like receptor signaling pathway were enriched between C5aR1 deficiency and wild-type mice. Mechanistically, C5aR1 deletion decreased the expression of TLR4 and NLRP3, subsequently regulating macrophage polarization. Moreover, C5aR1 antagonist PMX-53 treatment mitigated the progression of NASH in mice. CONCLUSIONS: Blockade of the C5a-C5aR1 axis reduces hepatic steatosis, inflammation, and fibrosis in NASH mice. Our data suggest that C5aR1 may be a potential target for drug development and therapeutic intervention of NASH.

Pentachlorophenol causes redox imbalance, inhibition of brush border membrane and metabolic enzymes, DNA damage and histological alterations in rat kidney.

Pentachlorophenol (PCP) is a synthetic organochlorine compound that is widely used in biocide and pesticide industries, and in preservation of wood, fence posts, cross arms and power line poles. Humans are usually exposed to PCP through air, contaminated water and food. PCP enters the body and adversely affects liver, gastrointestinal tract, kidney and lungs. PCP is a highly toxic class 2B or probable human carcinogen that produces large amount of reactive oxygen species (ROS) within cells. This work aimed to determine PCP-induced oxidative damage in rat kidney. Adult rats were given PCP (25, 50, 100, 150 mg/kg body weight), in corn oil, once a day for 5 days while control rats were given similar amount of corn oil by oral gavage. PCP increased hydrogen peroxide level and oxidation of thiols, proteins and lipids. The antioxidant status of kidney cells was compromised in PCP treated rats while enzymes of brush border membrane (BBM) and carbohydrate metabolism were inhibited. Plasma level of creatinine and urea was also increased. Administration of PCP increased DNA fragmentation, cross-linking of DNA to proteins and DNA strand scission in kidney. Histological studies supported biochemical findings and showed significant damage in the kidneys of PCP-treated rats. These changes could be due to redox imbalance or direct chemical modification by PCP or its metabolites. These results signify that PCP-induced oxidative stress causes nephrotoxicity, dysfunction of BBM enzymes and DNA damage.

Oxidized corn oil changes the liver lipid metabolism of broilers by upregulating peroxisome proliferators activate receptor-α.

The objective of the following study was to investigate the effects of naturally oxidized corn oil on the antioxidant capacity and lipid metabolism of broilers. A total of 450, 1-day-old Arbor Acres male broilers were randomly divided into 5 treatments with 6 replicate cages and 15 birds/cage. The dietary treatment array consisted of ratios of naturally oxidized corn oil to non-oxidized corn oil from 0:100, 25:75, 50:50, 75:25, and 100:0, respectively. Serum, liver, and abdominal fat samples were taken at 42 d. The results showed that the liver organ index, liver catalase (CAT) activity, malondialdehyde (MDA) content, and the serum aspartate aminotransferase (AST) content had significant quadratic relationships with the ratio of naturally oxidized corn oil (P < 0.05). Inflammatory infiltrating cells appeared in the liver of the 50% and 75% oxidized corn oil group. The percentage of abdominal fat, and serum free fatty acids (FFA) content increased linearly with the increased proportion of oxidized corn oil (P < 0.05). The mRNA expression of NADH quinone oxidoreductase 1 (NQO-1), nuclear factor kappa B (NF-κB), toll-like receptor-4 (TLR-4), peroxisome proliferators activate receptor-α (PPARα), carnitine acyltransferase (CPT1), and acyl-coenzyme oxidase (ACO) of the liver increased linearly while oxidized corn oil increased in the diet (P < 0.05). Diets containing 100% oxidized corn oil significantly changed the mRNA expression of liver Caveolin compared with other treatment groups (P < 0.05). Taken together, this study demonstrated that naturally oxidized corn oil could change liver lipid metabolism and accelerate lipid deposition of broilers by upregulating PPARα.

Monounsaturated fatty acid-enriched olive oil exacerbates chronic alcohol-induced hepatic steatosis and liver injury in C57BL/6J mice.

Dietary oil composition determines the pathological processes of alcoholic fatty liver disease (AFLD). Oil rich in saturated fatty acids protects, whereas oil rich in polyunsaturated fatty acids aggravates the alcohol-induced liver injury. However, limited studies have been conducted to address how monounsaturated fatty acids (MUFAs) enriched oil controls the pathological development of AFLD. Therefore, this study was designed to evaluate the effect of MUFA-enriched extra virgin olive oil (OO) on AFLD. Twenty C57BL/6J mice were randomly allocated into four groups and fed modified Lieber-DeCarli liquid diets containing isocaloric maltose dextrin a non-alcohol or alcohol with corn oil and OO for four weeks. Dietary OO significantly exacerbated alcohol-induced liver dysfunction, evidenced by histological examinations and disturbed biochemical parameters. Dietary OO with alcohol decreased hormone-sensitive lipase (HSL), phosphorylated 5'-AMP-activated protein kinase (p-AMPK), and carnitine palmitoyltransferase-Iα (CPT1α) expression, and increased sterol regulatory element-binding protein-1c (SREBP-1c), diacylglycerol acyltransferase-2 (DGAT2), and very low-density lipoprotein receptor (VLDLR) expression in the liver. It also promoted the expression of hepatic interleukin-6 (IL-6) and hepatic tumour necrosis factor-alpha (TNF-α) at the transcriptional level. Additionally, adipose tissue lipolysis partially had an etiologic effect on alcohol-induced hepatic steatosis under OO pretreatment. In conclusion, MUFA-enriched OO exacerbated liver dysfunction in vivo. OO should be cautiously considered as a unique dietary oil source for individuals with AFLD.

Oil-in-Water Nanoemulsion Can Modulate the Fermentation, Fatty Acid Accumulation, and the Microbial Population in Rumen Batch Cultures.

In this study, three oil-in-water nanoemulsions were tested in two stages: In the first stage, three levels (on the substrate dry matter (DM)), namely 3%, 6%, and 9%, of three different oils, olive oil (OO), corn oil (CO), and linseed oil (LO), in raw and nanoemulsified (N) forms were used separately in three consecutive rumen batch cultures trials. The second stage, which was based on the first stage's results, consisted of a batch culture trial that compared the raw and nanoemulsified (N) forms of all three oils together, provided at 3% of the DM. In the first stage, NOO, NCO, and NLO preserved higher unsaturated fatty acid (UFA) and less saturated fatty acid (SFA) compared to OO, CO, and LO, respectively; noticeably, NCO had UFA:SFA = 1.01, 1.16, and 1.34 compared to CO, which had UFA:SFA = 0.66, 0.69, and 0.72 when supplemented at 3%, 6%, 9% of DM, respectively. In the second stage, UFA:SFA = 1.04, 1.12, and 1.07 for NOO, NCO, NLO, as compared to UFA:SFA = 0.69, 0.68, and 0.72 for OO, CO, and LO supplemented at 3% of DM. In conclusion, oil-in-water nanoemulsions showed an ability to decrease the transformation of UFA to SFA in the biohydrogenation environment without affecting the rumen microorganisms.

Adverse effects of triclosan on kidney in mice: Implication of lipid metabolism disorders.

Triclosan (TCS) is a ubiquitous antimicrobial used in daily consumer products. Previous reports have shown that TCS could induce hepatotoxicity, endocrine disruption, disturbance on immune function and impaired thyroid function. Kidney is critical in the elimination of toxins, while the effects of TCS on kidney have not yet been well-characterized. The aim of the present study was to investigate the effects of TCS exposure on kidney function and the possible underlying mechanisms in mice. Male C57BL/6 mice were orally exposed to TCS with the doses of 10 and 100 mg/(kg•day) for 13 weeks. TCS was dissolved in dimethyl sulfoxide (DMSO) and diluted by corn oil for exposure. Corn oil containing DMSO was used as vehicle control. Serum and kidney tissues were collected for study. Biomarkers associated with kidney function, oxidative stress, inflammation and fibrosis were assessed. Our results showed that TCS could cause renal injury as was revealed by increased levels of renal function markers including serum creatinine, urea nitrogen and uric acid, as well as increased oxidative stress, pro-inflammatory cytokines and fibrotic markers in a dose dependent manner, which were more significantly in 100 mg/(kg•day) group. Mass spectrometry-based analysis of metabolites related with lipid metabolism demonstrated the occurrence of lipid accumulation and defective fatty acid oxidation in 100 mg/(kg•day) TCS-exposed mouse kidney. These processes might lead to lipotoxicity and energy depletion, thus resulting in kidney fibrosis and functional decline. Taken together, the present study demonstrated that TCS could induce lipid accumulation and fatty acid metabolism disturbance in mouse kidney, which might contribute to renal function impairment. The present study further widens our insights into the adverse effects of TCS.

Improving the in vitro and in vivo bioavailability of pterostilbene using Yesso scallop gonad protein isolates-epigallocatechin gallate (EGCG) conjugate-based emulsions: effects of carrier oil.

This study investigated the influence of carrier oils on the in vitro and in vivo bioavailability of PTE encapsulated in scallop gonad protein isolates (SGPIs)-epigallocatechin gallate (EGCG) conjugate stabilized emulsions. The SGPIs-EGCG stabilized emulsions were subjected to an in vitro simulated digestion, and the resulting corn oil and MCT micelles were used to evaluate the PTE transportation using the Caco-2 cell model. Both emulsions remarkably improved the bioaccessibility of PTE in the micelle phase. Nevertheless, corn oil emulsions increased trans-enterocyte transportation of PTE more efficiently than MCT emulsions. Furthermore, the maximum plasma concentrations of PTE and its metabolites in mice fed with PTE emulsions were prominently higher than those in mice fed with PTE solution, while the in vivo metabolic patterns of PTE in different oil-stabilized emulsions were different. Therefore, SGPIs-EGCG stabilized emulsions could enhance the bioavailability of PTE through controlled release, in which corn oil is more suitable than MCT.

3-Indolepropionic acid prevented chlorpyrifos-induced hepatorenal toxicities in rats by improving anti-inflammatory, antioxidant, and pro-apoptotic responses and abating DNA damage.

The application of chlorpyrifos (CPF), an organophosphorus pesticide to control insects, is associated with oxidative stress and reduced quality of life in humans and animals. Indole-3-propionic acid (IPA) is a by-product of tryptophan metabolism with high antioxidant capacity and has the potential to curb CPF-mediated toxicities in the hepatorenal system of rats. It is against this background that we explored the subacute exposure of CPF and the effect of IPA in the liver and kidney of thirty rats using five cohort experimental designs (n = 6) consisting of control (corn oil 2 mL/kg body weight), CPF alone (5 mg/kg), IPA alone (50 mg/kg), CPF + IPA1 (5 mg/kg + 25 mg/kg), and CPF + IPA2 (5 mg/kg + 50 mg/kg). Subsequently, we evaluated biomarkers of hepatorenal damage, oxidative and nitrosative stress, inflammation, DNA damage, and apoptosis by spectrophotometric and enzyme-linked immunosorbent assay methods. Our results showed that co-treatment with IPA decreased CPF-upregulated serum hepatic transaminases, creatinine, and urea; reversed CPF downregulation of SOD, CAT, GPx, GST, GSH, Trx, TRx-R, and TSH; and abated CPF upregulation of XO, MPO, RONS, and LPO. Co-treatment with IPA decreased CPF-upregulated IL-1ß and 8-OHdG levels, caspase-9 and caspase-3 activities, and increased IL-10. In addition, IPA averts CPF-induced histological changes in the liver and kidney of rats. Our results demonstrate that co-dosing CPF-exposed rats with IPA can significantly decrease CPF-induced oxidative stress, pro-inflammatory responses, DNA damage, and subsequent pro-apoptotic responses in rats' liver and kidneys. Therefore, supplementing tryptophan-derived endogenous IPA from exogenous sources may help avert toxicity occasioned by inadvertent exposure to harmful chemicals, including CPF-induced systemic perturbation of liver and kidney function.

A comparative study between olive oil and corn oil on oxidative metabolism.

Fats are an important part of diet, but not all lipids have the same structure and chemical properties. Unsaturated fatty acids have one or more double bonds in their structure and can be monounsaturated or polyunsaturated, respectively. Most vegetable oils, such as olive oil and corn oil, contain significant amounts of these fatty acids. The presence of double bonds in the molecule of a fatty acid constitutes vulnerable sites for oxidation reactions generating lipid peroxides, potentially toxic compounds that can cause cellular damage. In response to this oxidative damage, aerobic organisms have intracellular enzymatic antioxidant defense mechanisms. The aim of the present investigation was to study comparatively the effects of control liquid diets, of a defined composition, containing olive oil or corn oil as a lipid source respectively of monounsaturated and polyunsaturated fatty acids, on the oxidative metabolism of rats. Rats were divided into three groups which received a control animal feed diet (A.F.), olive oil liquid diet (O.O) and corn oil liquid diet (C.O) for 30 days. It was observed that the activity of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), increased in the liver and white fat tissue of rats fed with olive oil when compared to the corn oil group. However, in brown fat tissue and blood cells, the enzyme activities showed a tendency to decrease in the olive oil group. In addition, the effect of olive oil and corn oil on several glucose metabolism parameters (pyruvate, lactate, LDH, acetoacetate and beta-hydroxybutyrate) showed that corn oil impairs to a greater extent the cellular metabolism. All these results helped in concluding that some body tissues are more adversely affected than others by the administration of corn oil or olive oil, and their antioxidant defenses and cellular metabolism respond differently too.

Upregulation of 4-Hydroxynonenal Contributes to the Negative Effect of n-6 Polyunsaturated Fatty Acid on Alcohol-Induced Liver Injury and Hepatic Steatosis.

The present study aimed to investigate the effects of saturated fatty acids (SFA) and n-6 polyunsaturated fatty acids (PUFA) on alcoholic liver disease (ALD) and the underlying mechanisms. C57BL/6J male mice were randomly fed a corn oil or palm oil diet (rich in n-6 PUFA and SFA, respectively) with or without ethanol for four weeks (n = 10/group). A series of experiments in vitro with AML-12 hepatocyte were conducted to better elucidate the potential mechanisms underlying the phenomenon observed in animals. Compared with palm oil, corn oil aggravated alcohol-induced liver injury and hepatic steatosis, indicated by a histological analysis and significant elevations of plasma alanine aminotransferase and hepatic triacylglycerol (TG) level. Apoptosis-associated proteins in the ASK1-JNK pathway were significantly enhanced in the liver of mice from the corn oil + ethanol group than in the palm oil + ethanol group. The corn oil + ethanol diet also inhibited the activation of both AMPK and downstream protein acetyl-CoA carboxylase (ACC) and promoted the SREBP-1c expression, subsequently accelerating lipid synthesis. In addition, 4-hydroxynonenal (4-HNE) levels in plasma and liver were significantly upregulated in response to corn oil + ethanol feeding. Interestingly, the in vitro study showed that 4-HNE significantly attenuated cell viability, elevated the expression of cleaved-caspase 3 protein and TG level, and regulated key molecules in ASK1-JNK and AMPK pathways in a dose-dependent manner. In conclusion, the n-6 PUFA diet showed a negative effect on alcohol-induced liver injury and steatosis. It might be related to the upregulation of 4-HNE and subsequent changes of proteins, namely, ASK1, JNK, AMPK, ACC, and SREBP-1c.

Effects of dietary vitamin E and fat supplementation in growing-finishing swine fed to a heavy slaughter weight of 150 kg: I. Growth performance, lean growth, organ size, carcass characteristics, primal cuts, and pork quality.

The study aimed to assess the effect of vitamin E (VE) supplementation and fat source on growth performance, lean growth, organ size, carcass characteristics, and pork quality of pigs at a heavy slaughter weight of 150 kg. A total of 64 pigs (32 barrows and 32 gilts; 28.41 ± 0.83 kg) were blocked by sex and body weight, and randomly assigned to one of eight dietary treatments (n = 8 per treatment) in a 4 × 2 factorial arrangement with main effects of fat source (corn starch [CS; no fat added], 5% tallow [TW], 5% distiller's corn oil [DCO], and 5% coconut oil [CN]) and VE supplementation level (11 and 200 ppm). Five-phase diets were formulated to meet requirement estimates of NRC and fed to pigs with each period of 25 kg from 25 to 150 kg. Increasing dietary VE supplementation from 11 to 200 ppm tended to increase average daily gain (ADG) in phase 5 (P = 0.08), and gain to feed ratio (G/F) in phase 4 (P = 0.06) and phase 5 (P = 0.06) resulting in increased G/F in the overall period (P = 0.10). Compared with the pigs fed the CS diet in the overall period, the pigs fed DCO diets had greater ADG (P < 0.05), the pigs fed the TW and CN diets had lower average daily feed intake (P < 0.05), and the pigs fed the fat-added diets had greater G/F (P < 0.05). Belly firmness was greatest in the pigs fed the CN diet and lowest in those fed the DCO diet (P < 0.05). Increasing dietary VE level from 11 to 200 ppm increased absolute and relative liver weight, absolute ham yield (P < 0.05), and tended to increase the relative yield of picnic shoulder (P = 0.07) and ham (P = 0.06) and the pigs fed the corn oil diet tended to have greater belly yield (P = 0.08) than the other fat treatments. Increasing dietary VE level increased 45-min pH and ΔpH at slaughter but decreased a* value, chroma (P < 0.10), and belly depth (P < 0.05). However, no effects of VE supplementation and fat source were observed on the other carcass traits and meat quality measurements. In conclusion, increasing dietary VE level from 11 to 200 ppm slightly increased growth rate and feed efficiency in the late finishing periods, and the addition of fat increased feed efficiency and backfat thickness, decreased lean content, and altered belly firmness. While there were some effects of VE supplementation and fat source observed on organ weight, primal cuts, carcass traits, and meat quality, there was no strong evidence that VE supplementation and fat source materially affected these measurements except for belly firmness.

The study aimed to assess the effect of vitamin E (VE) supplementation and fat source on growth performance, carcass characteristics, and pork quality of pigs slaughtered at 150 kg. Fat sources included corn starch (no fat added), or 5% tallow, distiller's corn oil (DCO), or coconut oil (CN); VE supplementation levels were 11 and 200 ppm. Increasing dietary VE from 11 to 200 ppm tended to increase the efficiency of conversion of feed to body weight gain for the overall study period. The pigs fed the DCO diet had greater backfat depth at slaughter. Belly (from which bacon is made) firmness was greatest in the pigs fed the CN diet and lowest in those fed the DCO diet. In conclusion, increasing dietary VE levels from 11 to 200 ppm slightly increased growth rate and feed efficiency, and the addition of fat increased feed efficiency and backfat thickness, decreased lean muscle content, and altered belly firmness. While there were some effects of VE supplementation and fat source, there was no strong evidence that VE supplementation and fat source materially affected these measurements except for belly firmness.

Effects of progesterone and interferon tau on ovine endometrial phosphate, calcium, and vitamin D signaling†.

Given recent reports of expression of postnatal mineral transport regulators at the maternal-conceptus interface during the peri-implantation period, this study tested the hypothesis that progesterone (P4) and interferon tau (IFNT) regulate phosphate, calcium, and vitamin D signaling in the ovine endometrium. Mature Rambouillet ewes (n = 24) were surgically fitted with intrauterine catheters on day 7 of the estrous cycle. Ewes received daily intramuscular injections of 50 mg of P4 in corn oil vehicle and 75 mg of progesterone receptor antagonist (RU486) in corn oil from days 8 to 15, and twice-daily intrauterine injections of either control proteins (CX) or IFNT (25 µg/uterine horn/day) from days 11 to 15 resulting in four treatment groups: P4 + CX; P4 + IFNT; RU486 + P4 + CX; and RU486 + P4 + IFNT. On day 16, ewes were hysterectomized. RU486 + P4 + CX treated ewes had lower concentrations of 25 (OH) D in plasma than P4 + CX treated ewes (P < 0.05). Endometria from ewes treated with IFNT had greater expression of FGF23 (P < 0.01), S100A9 (P < 0.05), and S100A12 (P = 0.05) mRNAs and lower expression of ADAM10 mRNA (P < 0.01) than of ewes treated with CX proteins. Expression of FGF23 mRNA was greater in endometria of ewes that received RU486 + P4 + IFNT than in ewes that received RU486 + P4 + CX (hormone × protein interaction, P < 0.05). The expression of S100G mRNA was greater in endometria of ewes that received P4 + IFNT compared to ewes that received RU486 + P4 + IFNT (P < 0.05; hormone × protein interaction, P < 0.01). These data implicate P4 and IFNT in the regulation of phosphate, calcium, and vitamin D signaling during the peri-implantation period of pregnancy and provide a platform for continued mechanistic investigations.

Progesterone and interferon tau regulate expression of polyamine enzymes during the ovine peri-implantation period†.

Progesterone (P4) and interferon tau (IFNT) are important for establishment and maintenance of pregnancy in ruminants. Agmatine and polyamines (putrescine, spermidine, and spermine) have important roles in the survival, growth, and development of mammalian conceptuses. This study tested the hypothesis that P4 and/or IFNT stimulate the expression of genes and proteins involved in the metabolism and transport of polyamines in the ovine endometrium. Rambouillet ewes (n = 24) were surgically fitted with intrauterine catheters on Day 7 of the estrous cycle. They received daily intramuscular injections of 50 mg P4 in corn oil vehicle and/or 75-mg progesterone receptor antagonist (RU486) in corn oil vehicle from Days 8-15, and twice daily intrauterine injections (25 µg/uterine horn/day) of either control serum proteins (CX) or IFNT from Days 11-15, resulting in four treatment groups: (i) P4 + CX; (ii) P4 + IFNT; (iii) RU486 + P4 + CX; or (iv) RU486 + P4 + IFNT. On Day 16, ewes were hysterectomized. The total amounts of arginine, citrulline, ornithine, agmatine, and putrescine in uterine flushings were affected (P < 0.05) by P4 and/or IFNT. P4 increased endometrial expression of SLC22A2 (P < 0.01) and SLC22A3 (P < 0.05) mRNAs. IFNT affected endometrial expression of MAT2B (P < 0.001), SAT1 (P < 0.01), and SMOX (P < 0.05) mRNAs, independent of P4. IFNT increased the abundance of SRM protein in uterine luminal (LE), superficial glandular (sGE), and glandular epithelia (GE), as well as MAT2B protein in uterine LE and sGE. These results indicate that P4 and IFNT act synergistically to regulate the expression of key genes required for cell-specific metabolism and transport of polyamines in the ovine endometrium during the peri-implantation period of pregnancy.

The protective effect of chrysin against oxidative stress and organ toxicity in rats exposed to propetamphos.

The aim of this study was to investigate the protective efficacy of chrysin against propetamphos exposure. For this purpose, 2 to 3-month-old 40 male Wistar Albino rats were used. These animals were randomly assigned to four groups. The animals in the control group received the vehicle substance (corn oil) alone. Groups 2, 3 and 4 were administered with 50 mg/kg.bw/day of chrysin (in corn oil), 10 mg/kg.bw/day of propetamphos (in corn oil), and 10 mg/kg.bw/day of propetamphos plus 50 mg/kg.bw/day of chrysin, respectively, for 28 days. Some oxidative stress/lipid peroxidation parameters (MDA, SOD, CAT, GSH-Px, NO, glutathione) and serum biochemical parameters (triglyceride, cholesterol, creatinine, BUN, creatine phosphokinase, ALT, ALP and pseudocholinesterase) were analyzed in tissue/blood samples. Also, histopathological findings were observed. According to the data obtained, no significant alteration had occurred in these parameters and the histological findings in the group given chrysin alone, when compared to the control group. Significant unfavorable alterations were detected in the oxidative stress/lipid peroxidation/antioxidant status parameters, all biochemical parameters and histopathological findings of the group that received propetamphos alone. In the group that was given both chrysin and propetamphos, remedial/recovery alterations were observed in the oxidative stress/lipid peroxidation/antioxidant status values, serum biochemical parameters and histopathological findings, such that the values and histopathological findings showed partly similarity to those of the control group. In result, it is suggested that chrysin may provide protection against propetamphos exposure and propetamphos-induced organ damage in rats at a certain level.

A high extra-virgin olive oil diet induces changes in metabolic pathways of experimental mammary tumors.

Breast cancer is the most common malignancy in women worldwide, and environmental factors, especially diet, have a role in the etiology of this disease. This work aimed to investigate the influence of high fat diets (rich in corn oil or extra virgin olive oil -EVOO-) and the timing of dietary intervention (from weaning or after induction) on tumor metabolism in a seven,12-dimethylbenz[a]anthracene (DMBA)-induced breast cancer model in rat. The effects of lipids (oils and fatty acids) have also been investigated in MCF-7 cells. The results have confirmed different effects on tumor progression depending on the type of lipid. Molecular analysis at mRNA, protein and activity level of enzymes of the main metabolic pathways have also shown differences among groups. Thus, the animals fed with the EVOO-enriched diet developed tumors with less degree of clinical and morphological malignancy and showed modified glucose and mitochondrial metabolism when compared to the animals fed with the corn oil-enriched diet. Paradoxically, no clear influence on lipid metabolism by the high fat diets was observed. Considering previous studies on proliferation and apoptosis in the same samples, the results suggest that metabolic changes have a role in the molecular context that results in the modulation of different signaling pathways. Moreover, metabolic characteristics, without the context of other pathways, may not reflect tumor malignancy. The time of dietary intervention plays also a role, suggesting the importance of metabolic plasticity and the relation with mammary gland status when the tumor is induced.

Temporal Effects of Different Vehicles on Wound Healing Potentials of Quercetin: Biochemical, Molecular, and Histopathological Approaches.

Development of novel drugs or formulations to accelerate the wound healing process is the need of current era. Quercetin (Q), a bioflavonoid, at 0.3% concentration has showed some wound healing potential in our preliminary studies. The present study was aimed to explore the wound healing potential of 0.3% quercetin formulated in 3 different vehicles, that is, dimethyl sulfoxide (DMSO; 10%), ointment base, and corn oil. Ninety experimentally wounded rats were grouped in 6 groups. The 0.3% quercetin mixed with DMSO, ointment base, and corn oil was topically applied once daily for 21 days on the wounds of groups 2, 4, and 6, respectively. DMSO, ointment base, and corn oil alone was applied similarly in groups 1, 3, and 5, respectively. Gross evaluation and wound contraction results revealed accelerated wound closure in all quercetin-treated groups. The mRNA expressions of vascular endothelial growth factor, transforming growth factor-ß1, and interluekin-10 were markedly upregulated in healing tissues of quercetin-treated groups. Tumor necrosis factor-α mRNA expression and protein levels were lowered by quercetin treatment. Quercetin-treated groups also showed increased activities of SOD (superoxide dismutase) and catalase, and levels of total thiols in wound tissues on day 7. Levels of superoxide anion radicals and malondialdehyde were markedly lower in quercetin-treated groups. Histologically, wound sections of quercetin-treated groups showed early dominance of fibroblasts, increased blood vessels, marked collagen deposition, and regenerated epithelial layer. The significant effects were more pronounced in ointment + Q group among all the quercetin-treated groups. In conclusion, 0.3% quercetin mixed in ointment base produced the fastest and better wound healing in rats.

Genetic basis of maize kernel oil-related traits revealed by high-density SNP markers in a recombinant inbred line population.

BACKGROUND: Maize (Zea mays ssp. mays) is the most abundantly cultivated and highly valued food commodity in the world. Oil from maize kernels is highly nutritious and important for the diet and health of humans, and it can be used as a source of bioenergy. A better understanding of genetic basis for maize kernel oil can help improve the oil content and quality when applied in breeding. RESULTS: In this study, a KUI3/SC55 recombinant inbred line (RIL) population, consisting of 180 individuals was constructed from a cross between inbred lines KUI3 and SC55. We phenotyped 19 oil-related traits and subsequently dissected the genetic architecture of oil-related traits in maize kernels based on a high-density genetic map. In total, 62 quantitative trait loci (QTLs), with 2 to 5 QTLs per trait, were detected in the KUI3/SC55 RIL population. Each QTL accounted for 6.7% (qSTOL1) to 31.02% (qBELI6) of phenotypic variation and the total phenotypic variation explained (PVE) of all detected QTLs for each trait ranged from 12.5% (OIL) to 52.5% (C16:0/C16:1). Of all these identified QTLs, only 5 were major QTLs located in three genomic regions on chromosome 6 and 9. In addition, two pairs of epistatic QTLs with additive effects were detected and they explained 3.3 and 2.4% of the phenotypic variation, respectively. Colocalization with a previous GWAS on oil-related traits, identified 19 genes. Of these genes, two important candidate genes, GRMZM2G101515 and GRMZM2G022558, were further verified to be associated with C20:0/C22:0 and C18:0/C20:0, respectively, according to a gene-based association analysis. The first gene encodes a kinase-related protein with unknown function, while the second gene encodes fatty acid elongase 2 (fae2) and directly participates in the biosynthesis of very long chain fatty acids in Arabidopsis. CONCLUSIONS: Our results provide insights on the genetic basis of oil-related traits and a theoretical basis for improving maize quality by marker-assisted selection.