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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

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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.

To elucidate the effect of rice protein (RP) on the depression of inflammation, growing and adult rats were fed with caseins and RP for 2 weeks. Compared with casein, RP reduced hepatic accumulations of reactive oxygen species (ROS) and nitro oxide (NO), and plasma activities of alanine transaminase (ALT) and aspartate transaminase (AST) in growing and adult rats. Intake of RP led to increased mRNA levels, and protein expressions of phosphoinositide 3 kinase (PI3K), protein kinase B (Akt), nuclear factor-κB 1 (NF-αB1), reticuloendotheliosis viral oncogene homolog A (RelA), tumor necrotic factor α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and monocyte chemoattractant protein-1 (MCP-1) were decreased, whereas hepatic expressions of interleukin-10 (IL-10) and heme oxygenase 1 (HO-1) were increased by RP. The activation of NF-κB was suppressed by RP through upregulation of inhibitory κB α (IκBα), resulting in decreased translocation of nuclear factor-κB 1 (p50) and RelA (p65) to the nucleus in RP groups. The present study demonstrates that RP exerts an anti-inflammatory effect to inhibit ROS-derived inflammation through suppression of the NF-κB pathway in growing and adult rats. Results suggest that the anti-inflammatory capacity of RP is independent of age.

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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

Methionine sulfoxide reductase (Msr) and glutathione (GSH) are two endogenous antioxidant systems for depressing oxidative stress. The aim of this study is to investigate the role of methionine in involving the stimulation of endogenous antioxidant capacity of rice protein (RP). Seven‐week‐old male Wistar rats (body weight 180–200 g) were fed with commercial pellets (as control), methionine, and RP for 2 weeks. Compared with control, GSH synthesis and expressions of MsrA, MsrB2, and MsrB3 were stimulated by methionine and RP. After 2 weeks of feeding, Nrf2 was activated by RP and methionine, whereas the expressions of Keap1 and Cul3 were depressed. The ARE‐driven antioxidant expressions (GCLC, GCLM, GS, HO‐1, NQO1, CAT, SOD, GR, GST, GPx) were upregulated by methionine and RP. Results suggest that the endogenous antioxidant response induced by RP is primarily attributed to the methionine availability, in which the stimulation of Msr and GSH antioxidant system via Nrf2‐ARE pathway. Practical applications Rice protein is a major plant protein, which is rich in sulfur‐containing amino acids and widely consumed in the world. This paper emphasizes that the amino acid plays a key role in inducing the antioxidant activity of rice protein. The present study provides an insight that the methionine availability of rice protein will be a useful target for health promoting by activating endogenous antioxidant response against ROS‐induced oxidative damage.