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4‐Hydroxy‐2‐nonenal (HNE) is an inducer of inflammation. The aim of this study was to elicit the link between the inhibition of HNE accumulation and the depression of inflammation whether dependent onl‐arginine availability in growing rats. Male Wistar rats were fed with different levels of l‐arginine at 250, 500, and 1000 mg/kg body weight for 14 days. The control group was fed with commercial pellets. After 14 days of oral administration, l‐arginine significantly reduced hepatic accumulation of HNE and depressed inflammation in rats as compared with the control group. Compared to the control group, the anti‐inflammatory action of l‐arginine is reflected by upregulation of hepatic interleukin‐10 (IL‐10) and the suppression of hepatic cyclooxygenase‐2, tumor necrotic factor α, IL‐1β, and IL‐6 expressions in growing rats. With l‐arginine administration, the activation of nuclear factor‐κB (NF‐κB) was efficaciously inhibited through the upregulation of inhibitory κBα, and the depression of phosphoinositide 3‐kinase/protein kinase B (PI3K/Akt). In conclusion, this study demonstrated that l‐arginine could reduce hepatic HNE levels and depress inflammation in growing rats, revealing a link between the inhibition of HNE accumulation with the depression of inflammation, which was attributed to the availability of l‐arginine. A significant finding of this study was that the anti‐inflammatory mechanism exerted by l‐arginine was to inhibit NF‐κB activation via downregulating PI3K/Akt. [ABSTRACT FROM AUTHOR]

BACKGROUND: Reactive oxygen species (ROS) can cause DNA damage. Rice protein (RP) inhibits ROS accumulation. However, a link between the reduction of ROS‐derived DNA damage and the intake of RP is far from clear. The main objective of this study is to elucidate the effects of RPs on the reduction of DNA damage in growing and adult rats. RESULTS: An intake of RP for 2 weeks significantly reduced the hepatic accumulation of ROS and 8‐hydroxydeoxyguanosine (8‐OHdG) in growing and adult rats, whereas the hepatic p53 content was markedly increased by RPs. After 2 weeks' feeding, the mRNA levels and protein expressions of p53, ataxia‐telangiectasia mutated (ATM), and Checkpoint kinase 2 (Chk2) were up‐regulated by RPs, whereas Murine Double Minute 2 (MDM2) expressions were markedly inhibited by RPs, resulting in more p53 being translocated into the nucleus. Nuclear factor erythroid 2 (NF‐E2)‐related factor 2 (Nrf2) was activated by RP by reducing Kelch‐like ECH‐associated protein 1 (Keap1), resulting in the up‐regulation of antioxidant expressions of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) in RP groups. CONCLUSION: Rice protein can exert an endogenous antioxidant activity to reduce ROS‐derived DNA damage by activating the Nrf2‐Keap1 pathway. This study suggests that the activation of the ATM‐Chk2‐p53 pathway might be one of the mechanisms exerted by RP for reducing DNA damage in growing and adult rats. © 2019 Society of Chemical Industry [ABSTRACT FROM AUTHOR]

BACKGROUND Methionine is an essential sulfur‐containing amino acid. To elucidate the influence of l‐methionine on activation of the nuclear factor erythroid 2‐related factor 2–antioxidant responsive element (Nrf2‐ARE) antioxidant pathway to stimulate the endogenous antioxidant activity for depressing reactive oxygen species (ROS)‐derived oxidative stress, male Wistar rats were orally administered l‐methionine daily for 14 days. RESULTS: With the intake of l‐methionine, Nrf2 was activated by l‐methionine through depressing Keap1 and Cul3, resulting in upregulation of ARE‐driven antioxidant expression (glutamate cysteine ligase catalytic subunit, glutamate cysteine ligase modulatory subunit, glutathione synthase (GS), catalase (CAT), superoxide dismutase (SOD), heme oxygenase 1, NAD(P)H:quinone oxidoreductase 1, glutathione reductase (GR), glutathione S‐transferase (GST), glutathione peroxidase (GPx)) with increasing l‐methionine availability. Upon activation of Nrf2, glutathione synthesis was increased through upregulated expression of methionine adenosyltransferase, S‐adenosylhomocysteine hydrolase, cystathionine β‐synthase, cystathionine γ‐lyse, glutamate cysteine ligase (GCL) and GS, while hepatic expressions of methionine sulfoxide reductases (MsrA, MsrB2, MsrB3) and hepatic enzyme activities (CAT, SOD, GCL, GR, GST, GPx) were uniformly stimulated with increasing consumption of l‐methionine. As a result, hepatic content of ROS and MDA were effectively reduced by l‐methionine intake. CONCLUSION: The present study demonstrates that methionine availability plays a critical role in activation of the Nrf2‐ARE pathway to induce an endogenous antioxidant response for depressing ROS‐derived oxidative stress, which is primarily attributed to the stimulation of methionine sulfoxide reductase expression and glutathione synthesis. © 2019 Society of Chemical Industry [ABSTRACT FROM AUTHOR]

BACKGROUND To elucidate whether and how alkali treatment, which is a common process for rice protein ( RP) extraction, affects antioxidant activity of RP, the different degree of alkali (from 0.1% to 0.4% of NaOH) was used to extract RP ( RP-1, RP-2, RP-3, RP-4). RESULTS The antioxidant capacities of scavenging free radicals [2,2′-azinobis(3-ethylbenzothiazoline-6-sulfonic acid] diammonium salt, ABTS; 1,1-diphenyl-2-picrylhydrazyl, DPPH), chelating metals (iron, copper) and reducing power investigated in the hydrolysates of RPs ( RP-1, RP-2, RP-3, RP-4) during in vitro pepsin-pancreatin digestion were effectively affected by alkali treatment. The present study demonstrated that the weakest antioxidant responses to ABTS radical-scavenging activity, DPPH radical-scavenging activity, iron chelating activity, copper chelating activity and reducing power were produced by RP-4 extracted by the highest alkali proportion (0.4% NaOH). CONCULSION The present study indicates that antioxidant capacity of RP could be more readily depressed by strict alkali degree and affected by gastrointestinal proteases. Results suggest that alkali extraction is a vital process to regulate the antioxidant activity of RP through modifying the compositions of amino acids, which are dependent on alkali magnitude. © 2016 Society of Chemical Industry [ABSTRACT FROM AUTHOR]