The objective of this study was to evaluate alterations in serum metabolites of transition dairy cows affected by biotin (BIO) and nicotinamide (NAM) supplementation. A total of 40 multiparous Holsteins were paired and assigned randomly within a block to one of the following four treatments: control (T), 30 mg/day BIO (T), 45 g/day NAM (T), and 30 mg/day BIO + 45 g/day NAM (T). Supplemental BIO and NAM were drenched on cows from 14 days before the expected calving date. Gas chromatography time-of-flight/mass spectrometry was used to analyze serum samples collected from eight cows in every groups at 14 days after calving. In comparison to T, T, T, and T had higher serum glucose concentrations, while non-esterified fatty acid in T and T and triglyceride in T were lower. Adenosine 5'-triphosphate was significantly increased in T. Both T and T had higher glutathione and lower reactive oxygen species. Moreover, T significantly increased inosine and guanosine concentrations, decreased β-alanine, etc. Certain fatty acid concentrations (including linoleic acid, oleic acid, etc.) were significantly decreased in both T and T. Some amino acid derivatives (spermidine in T, putrescine and 4-hydroxyphenylethanol in T, and guanidinosuccinic acid in both T and T) were affected. Correlation network analysis revealed that the metabolites altered by NAM supplementation were more complicated than those by BIO supplementation. These findings showed that both BIO and NAM supplementation enhanced amino acid metabolism and NAM supplementation altered biosynthesis of unsaturated fatty acid metabolism. The improved oxidative status and glutathione metabolism further indicated the effect of NAM on oxidative stress alleviation.

The intestinal epithelium is susceptible to heat stress (HS), which leads to gut leakage and inflammation. However, the mechanisms underlying HS-induced intestine dysfunction have yet to be elucidated. We established an in vitro chronic heat exposure-induced intestinal injury of intestinal porcine epithelial cells (IPEC-J2) exposed to high temperatures (43 °C) for 12 h. The results revealed that HS increased reactive oxygen species (ROS) generation and decreased superoxide dismutase 2 (SOD2) expression, leading to oxidative stress. Western blotting analysis demonstrated that HS induced apoptosis as evidenced by increased cytochrome c (Cyt c) release in the cytoplasm and caspase 3 activation. Transcriptome sequencing analysis revealed that HS activated the endoplasmic reticulum stress (ERS) response/unfolded protein response (UPR) but inhibited glutathione metabolism. Specifically, HS triggered the pro-apoptotic activating transcription factor 4 (ATF4)/CEBP-homologous protein (CHOP) branch of the UPR. Interestingly, glutathione-specific gamma-glutamylcyclotransferase1 (CHAC1) involved in glutathione degradation was upregulated due to heat exposure and was proved to be downstream of the ATF4–CHOP signal pathway. Knockdown of CHAC1 attenuated the HS-induced decrease in glutathione level and cell apoptosis. These studies suggest that crosstalk between ERS and oxidative stress in HS-induced apoptosis might be dependent on the ATF4–CHOP–CHAC1 signal pathway in IPEC-J2 cells.

Subacute ruminal acidosis (SARA) continues to be a common and costly metabolic disorder in highproducing dairy cows worldwide. The objective of this study was to evaluate if increasing the concentration of physically effective neutral detergent fiber (peNDF) in diets can reduce the risk of SARA in cows fed a highconcentrate diet. Thirty second-parity Holstein cows in mid lactation (131 ± 8.3 d in milk) were randomly allocated to 3 dietary treatments (10 dairy cows per group): high (11.3%, high peNDF 8.0 ), medium (10.6%, medium peNDF 8.0 ), or low (9.0%, low peNDF 8.0 ) concentration of peNDF 8.0 . The diets were prepared by mixing the same total mixed ration (57% concentrate and 43% roughages) for 10, 18, or 60 min, respectively. The treatments were fed for 36 d with 21 d for adaptation and 15 d for sampling. The peNDF 8.0 intake was positively correlated with the peNDF 8.0 concentration. Chewing and ruminating times adjusted for dry matter intake and NDF intake were linearly increased with the increased dietary peNDF 8.0 concentration. The high peNDF 8.0 diet decreased the number of meals per day. The increased dietary peNDF 8.0 concentration linearly increased the rumen fluid pH, the molar percentage of acetate and isobutyrate, acetate-to-propionate ratio, and ammonia nitrogen concentration, but linearly decreased the molar percentages of propionate and valerate. The total VFA concentration and the molar percentages of butyrate and isovalerate remained unchanged. Meanwhile, the increase in the peNDF 8.0 concentration of the diet linearly increased the activities of carboxymethyl cellulase, avicelase, β-glucanase, and ferulic acid esterase in rumen fluid, but did not affect the activities of xylanase. Total plasma antioxidant capacity, γ-glutamyl transpeptidase activity, and plasma concentrations of total protein, albumin, creatinine, and malondialdehyde were linearly decreased by the increased dietary peNDF 8.0 concentration. The increase in peNDF 8.0 concentration raised the plasma concentrations of glucose, triglyceride, cholesterol, and blood urea nitrogen. Somatic cell counts in the milk were positively correlated with the dietary peNDF 8.0 concentration. The feed and milk energy efficiencies were unaffected by the treatments. Shortening the total mixed ration mixing time may be a practical strategy to increase the peNDF 8.0 concentration and reduce the risk of SARA in dairy cows fed high-concentrate diets.

The growth and health statuses of calves during the early stages of development have a significant effect on milk production during their first lactation period. Using appropriate milk replacers helps meet the long-term targets of dairy farmers. This study aimed to examine the effects of milk, milk replacer, and milk replacer plus ethoxyquin on growth performance, antioxidant status, immune function, and the gut microbiota of Holstein dairy calves. A total of 36 neonatal dairy calves were randomly divided into three groups and fed different diets: one group was fed milk, another group was fed milk replacer, and the third group was given milk replacer plus ethoxyquin. The supplementation with ethoxyquin was started on day 35 of the feeding period. The calves were weaned on day 45, and the experiment was conducted until day 49. The blood and fecal samples were collected at the end of the animal experiment. The results showed that milk replacers induced poor growth performance (body weight and average daily gain). However, milk replacer plus ethoxyquin aided in growth performance, enhanced the starter intake and blood antioxidative ability, and elevated the concentration of fecal valeric acid. Moreover, fecal fermentation and 16S rRNA analyses showed that milk replacer plus ethoxyquin altered the microbial composition (reducing Alistipes and Ruminococcaceae and increasing Bacteroides and Alloprevotella). Pearson's correlation assays showed that alterations in fecal microbiota strongly correlated with average daily gain and antioxidative ability. The results indicated the potential of milk replacer plus ethoxyquin in modulating the growth of dairy calves and in enhancing their ability to combat stress.

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BACKGROUND The present study aimed to investigate whether leucine (Leu) alleviates oxidative injury in bovine intestinal epithelial cells (BIECs) induced by hydrogen peroxide (H2O2), as well as the underlying molecular mechanisms. RESULTS BIECs were treated with H2O2 (1 mmol L−1) and/or Leu (0, 0.9, 1.8 or 3.6 mmol L−1) for 2 h. Leu increased cell viability (P < 0.05) and decreased the release of lactate dehydrogenase (P < 0.05) in BIECs challenged by H2O2. Then, the cells were treated with H2O2 (1 mmol L−1) and/or Leu (1.8 mmol L−1) for 2 h. Compared with the H2O2 group, cells treated with Leu and Leu + H2O2 exhibited increased (P < 0.05) mRNA and protein expression of superoxide dismutase 2 (SOD2), catalase (CAT), glutathione peroxidase 1 (GPx1), heme oxygenase 1 (HO‐1) and nuclear factor erythroid 2‐related factor 2 (Nrf2). BIECs treatment with Leu significantly reduced (P < 0.05) apoptosis induced by H2O2. BIECs were transfected with Nrf2 small interfering RNA (siRNA) for 48 h and/or treated with H2O2 (1 mmol L−1) and/or Leu (1.8 mmol L−1) for another 2 h. Transfection with Nrf2 siRNA abrogated the protective effect of Leu against H2O2‐induced apoptosis and the mRNA and protein expression of SOD2 (P < 0.05). CONCLUSION These results indicate that Leu promotes the relative expression of antioxidant enzymes (SOD2, CAT and GPx1) and phase II detoxification enzymes (HO‐1) by upregulating nuclear Nrf2 and activating the Nrf2 signaling pathway, thus enhancing the antioxidant capacity of cells. © 2022 Society of Chemical Industry.

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