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Ruchika Tandon - One of the best experts on this subject based on the ideXlab platform.

  • Hyperhomocysteinemia induced locked-in syndrome in a young adult due to Folic Acid Deficiency.
    Nutritional Neuroscience, 2019
    Co-Authors: Satyendra Kumar Sonkar, Satish Kumar, Neeraj Kumar Singh, Ruchika Tandon
    Abstract:

    'Locked-in syndrome (LIS)' is a neurological disorder, often missed initially and can have grave consequences. A rare case of LIS caused due to Folic Acid Deficiency-induced hyperhomocysteinemia is being described here. A 16-year-old boy presented with complaints of sudden onset weakness of all the four limbs with loss of voice for one day. All the tendon reflexes were increased, bilateral planters were extensor and sensory system was intact. Patient was conscious and responded to verbal commands by ocular movements in vertical direction. Hence, a diagnosis of LIS was made. Magnetic resonance imaging of the head revealed an acute infarct in ventral pons. Serum homocysteine level was elevated (20.65 μmol/l) and Folic Acid level was severely low (1.7 nmol/ml). Cause of LIS was found to be hyperhomocysteinemia induced stroke in the pons, related to Folic Acid Deficiency. The patient was managed with antiplatelet agents and Folic Acid supplementation and was discharged subsequently. Recognition of LIS is important as casual remarks at bedside can severely traumatize an already paralyzed but conscious and awake patient. Folic Acid Deficiency can lead to hyperhomocysteinemia, which can cause strokes and even LIS. Prevention of hyperhomocysteinemia may possibly prevent such neurological disasters.

  • hyperhomocysteinemia induced locked in syndrome in a young adult due to Folic Acid Deficiency
    Nutritional Neuroscience, 2019
    Co-Authors: Satyendra Kumar Sonkar, Satish Kumar, Neeraj Kumar Singh, Ruchika Tandon
    Abstract:

    ‘Locked-in syndrome (LIS)’ is a neurological disorder, often missed initially and can have grave consequences. A rare case of LIS caused due to Folic Acid Deficiency-induced hyperhomocysteinemia is...

Satyendra Kumar Sonkar - One of the best experts on this subject based on the ideXlab platform.

  • Hyperhomocysteinemia induced locked-in syndrome in a young adult due to Folic Acid Deficiency.
    Nutritional Neuroscience, 2019
    Co-Authors: Satyendra Kumar Sonkar, Satish Kumar, Neeraj Kumar Singh, Ruchika Tandon
    Abstract:

    'Locked-in syndrome (LIS)' is a neurological disorder, often missed initially and can have grave consequences. A rare case of LIS caused due to Folic Acid Deficiency-induced hyperhomocysteinemia is being described here. A 16-year-old boy presented with complaints of sudden onset weakness of all the four limbs with loss of voice for one day. All the tendon reflexes were increased, bilateral planters were extensor and sensory system was intact. Patient was conscious and responded to verbal commands by ocular movements in vertical direction. Hence, a diagnosis of LIS was made. Magnetic resonance imaging of the head revealed an acute infarct in ventral pons. Serum homocysteine level was elevated (20.65 μmol/l) and Folic Acid level was severely low (1.7 nmol/ml). Cause of LIS was found to be hyperhomocysteinemia induced stroke in the pons, related to Folic Acid Deficiency. The patient was managed with antiplatelet agents and Folic Acid supplementation and was discharged subsequently. Recognition of LIS is important as casual remarks at bedside can severely traumatize an already paralyzed but conscious and awake patient. Folic Acid Deficiency can lead to hyperhomocysteinemia, which can cause strokes and even LIS. Prevention of hyperhomocysteinemia may possibly prevent such neurological disasters.

  • hyperhomocysteinemia induced locked in syndrome in a young adult due to Folic Acid Deficiency
    Nutritional Neuroscience, 2019
    Co-Authors: Satyendra Kumar Sonkar, Satish Kumar, Neeraj Kumar Singh, Ruchika Tandon
    Abstract:

    ‘Locked-in syndrome (LIS)’ is a neurological disorder, often missed initially and can have grave consequences. A rare case of LIS caused due to Folic Acid Deficiency-induced hyperhomocysteinemia is...

Sheng-yao Kuang - One of the best experts on this subject based on the ideXlab platform.

  • immunity decreases antioxidant system damages and tight junction changes in the intestine of grass carp ctenopharyngodon idella during Folic Acid Deficiency regulation of nf κb nrf2 and mlck mrna levels
    Fish & Shellfish Immunology, 2016
    Co-Authors: Lei Shi, Lin Feng, Wei-dan Jiang, Yang Liu, Jun Jiang, Sheng-yao Kuang
    Abstract:

    This investigation used the same growth trial as the previous study, which showed that Folic Acid Deficiency retarded growth in young grass carp (the percent weight gain of Groups 1-6 were 102.32 ± 3.41%, 137.25 ± 10.48%, 179.78 ± 3.95%, 164.33 ± 3.21%, 143.35 ± 8.12% and 115.28 ± 2.66%) [1]. In the present study, we investigated the effects of dietary Folic Acid on the immune response, antioxidant status and tight junctions in the intestine of young grass carp (Ctenopharyngodon idella). A total of 540 young grass carp were fed diets containing graded levels of Folic Acid at 0.10, 0.47, 1.03, 1.48, 1.88 and 3.12 mg kg(-1) diet for 8 weeks. The results indicated that Acid phosphatase and lysozyme activities, and the complement component 3 content in the proximal intestine (PI), mid intestine (MI) and distal intestine (DI) were decreased with Folic Acid Deficiency (0.1 mg kg(-1)) (P < 0.05). Folic Acid Deficiency (0.1 mg kg(-1)) up-regulated interleukin 1β, interleukin 8, tumor necrosis factor α, nuclear factor κB p65 (NF-κB p65), IκB kinase α (IKK-α), IKK-β and IKK-γ gene expression, meanwhile down-regulated interleukin 10, transforming growth factor β, IκB and target of rapamycin gene expression in the PI, MI and DI (P < 0.05). These data suggested that Folic Acid Deficiency decreased fish intestinal innate immune function may be partly contributed to the regulation of NF-κB p65 pathway. Moreover, the activities and corresponding gene expression of glutathione content, Cu/Zn superoxide dismutase, catalase, glutathione peroxidase, glutathione s-transferases and glutathione reductase in fish intestine were depressed by deficient Folic Acid diet (0.1 mg kg(-1)) (P < 0.05). Furthermore, Folic Acid Deficiency (0.1 mg kg(-1)) down-regulated NF-E2-related factor 2 (Nrf2) gene expression, up-regulated Kelch-like-ECH-associated protein 1a (Keap1a) and Keap1b gene expression in fish intestine (P < 0.05). These data indicated that deficient Folic Acid diet damaged fish intestinal antioxidant capacity partly by regulating Nrf2/Keap1 pathway. Additionally, Folic Acid Deficiency (0.1 mg kg(-1)) down-regulated claudin-b, claudin-c, claudin-3, occludin and zonula occludens 1 gene expression; whereas Folic Acid Deficiency (0.1 mg kg(-1)) up-regulated claudin-12, claudin-15, myosin light chain kinase (MLCK) and p38 mitogen activated protein kinase (p38 MAPK) gene expression in the PI, MI and DI (P < 0.05), suggesting that Folic Acid Deficiency may damage fish intestinal tight junctions associated with the mediation of MLCK and p38 MAPK gene expression. In conclusion, Folic Acid Deficiency (0.1 mg kg(-1)) impaired fish intestinal immunity, antioxidant capacity and tight junctions.

  • Immunity decreases, antioxidant system damages and tight junction changes in the intestine of grass carp (Ctenopharyngodon idella) during Folic Acid Deficiency: Regulation of NF-κB, Nrf2 and MLCK mRNA levels.
    Fish & Shellfish Immunology, 2016
    Co-Authors: Lei Shi, Lin Feng, Wei-dan Jiang, Yang Liu, Jun Jiang, Sheng-yao Kuang, Ling Tang, Wu-neng Tang, Yong-an Zhang
    Abstract:

    This investigation used the same growth trial as the previous study, which showed that Folic Acid Deficiency retarded growth in young grass carp (the percent weight gain of Groups 1-6 were 102.32 ± 3.41%, 137.25 ± 10.48%, 179.78 ± 3.95%, 164.33 ± 3.21%, 143.35 ± 8.12% and 115.28 ± 2.66%) [1]. In the present study, we investigated the effects of dietary Folic Acid on the immune response, antioxidant status and tight junctions in the intestine of young grass carp (Ctenopharyngodon idella). A total of 540 young grass carp were fed diets containing graded levels of Folic Acid at 0.10, 0.47, 1.03, 1.48, 1.88 and 3.12 mg kg(-1) diet for 8 weeks. The results indicated that Acid phosphatase and lysozyme activities, and the complement component 3 content in the proximal intestine (PI), mid intestine (MI) and distal intestine (DI) were decreased with Folic Acid Deficiency (0.1 mg kg(-1)) (P 

  • Folic Acid Deficiency impairs the gill health status associated with the NF-κB, MLCK and Nrf2 signaling pathways in the gills of young grass carp (Ctenopharyngodon idella).
    Fish & Shellfish Immunology, 2015
    Co-Authors: Lei Shi, Lin Feng, Wei-dan Jiang, Yang Liu, Jun Jiang, Juan Zhao, Sheng-yao Kuang, Ling Tang, Wu-neng Tang
    Abstract:

    The aim of this study was to investigate the effect of dietary Folic Acid on fish growth, the immune and barrier functions of fish gills, and the potential mechanisms of these effects. Young grass carp (Ctenophatyngodon idella) were fed diets containing graded levels of Folic Acid at 0.10 (basal diet), 0.47, 1.03, 1.48, 1.88 and 3.12 mg kg(-1) diet for 8 weeks. The results showed that Acid phosphatase and lysozyme activities and the complement component 3 content in fish gills decreased with Folic Acid Deficiency (P < 0.05). Folic Acid Deficiency up-regulated liver-expressed antimicrobial peptide 1, interleukin 1 beta, interleukin 8, tumor necrosis factor alpha, nuclear factor kappa B p65, I kappa B kinase alpha (IKK-alpha), IKK-beta and IKK-gamma gene expression. Folic Acid Deficiency down-regulated interleukin 10, transforming growth factor beta, I kappa B and target of rapamycin gene expression in fish gills (P < 0.05). These results showed that limited Folic Acid decreased fish gill immune status. Furthermore, Folic Acid Deficiency down-regulated claudin-b, claudin-c, claudin-3, occludin and zonula occludens 1 gene expression, whereas Folic Acid Deficiency up-regulated claudin-12, claudin-15, myosin light chain kinase and p38 mitogen activated protein kinase gene expression in fish gills (P < 0.05). These results suggested that Folic Acid Deficiency disrupted tight junction-mediated fish gill barrier function. Additionally, Folic Acid Deficiency increased the content of reactive oxygen species, protein carbonyl and malondialdehyde (MDA); Mn superoxide dismutase activity and gene expression; and Kelch-like-ECH-associated protein 1a (Keap1a) and Keap1b gene expression (P < 0.05). Conversely, Folic Acid Deficiency decreased Cu/Zn superoxide dismutase, catalase, glutathione peroxidase, glutathione s-transferases and glutathione reductase activities and gene expression as well as NF-E2-related factor 2 gene expression in fish gills (P < 0.05). All of these results indicated that Folic Acid Deficiency impaired fish gill health status via regulating gene expression of cytokines, tight junction proteins, antioxidant enzymes, NF-kappa B p65, MLCK and Nrf2. Based on percent weight gain, LZ activity and MDA content in the gills, the dietary Folic Acid requirements for young grass carp were 1.60, 2.07 and 2.08 mg kg(-1), respectively. (C) 2015 Published by Elsevier Ltd.

Jun Jiang - One of the best experts on this subject based on the ideXlab platform.

  • immunity decreases antioxidant system damages and tight junction changes in the intestine of grass carp ctenopharyngodon idella during Folic Acid Deficiency regulation of nf κb nrf2 and mlck mrna levels
    Fish & Shellfish Immunology, 2016
    Co-Authors: Lei Shi, Lin Feng, Wei-dan Jiang, Yang Liu, Jun Jiang, Sheng-yao Kuang
    Abstract:

    This investigation used the same growth trial as the previous study, which showed that Folic Acid Deficiency retarded growth in young grass carp (the percent weight gain of Groups 1-6 were 102.32 ± 3.41%, 137.25 ± 10.48%, 179.78 ± 3.95%, 164.33 ± 3.21%, 143.35 ± 8.12% and 115.28 ± 2.66%) [1]. In the present study, we investigated the effects of dietary Folic Acid on the immune response, antioxidant status and tight junctions in the intestine of young grass carp (Ctenopharyngodon idella). A total of 540 young grass carp were fed diets containing graded levels of Folic Acid at 0.10, 0.47, 1.03, 1.48, 1.88 and 3.12 mg kg(-1) diet for 8 weeks. The results indicated that Acid phosphatase and lysozyme activities, and the complement component 3 content in the proximal intestine (PI), mid intestine (MI) and distal intestine (DI) were decreased with Folic Acid Deficiency (0.1 mg kg(-1)) (P < 0.05). Folic Acid Deficiency (0.1 mg kg(-1)) up-regulated interleukin 1β, interleukin 8, tumor necrosis factor α, nuclear factor κB p65 (NF-κB p65), IκB kinase α (IKK-α), IKK-β and IKK-γ gene expression, meanwhile down-regulated interleukin 10, transforming growth factor β, IκB and target of rapamycin gene expression in the PI, MI and DI (P < 0.05). These data suggested that Folic Acid Deficiency decreased fish intestinal innate immune function may be partly contributed to the regulation of NF-κB p65 pathway. Moreover, the activities and corresponding gene expression of glutathione content, Cu/Zn superoxide dismutase, catalase, glutathione peroxidase, glutathione s-transferases and glutathione reductase in fish intestine were depressed by deficient Folic Acid diet (0.1 mg kg(-1)) (P < 0.05). Furthermore, Folic Acid Deficiency (0.1 mg kg(-1)) down-regulated NF-E2-related factor 2 (Nrf2) gene expression, up-regulated Kelch-like-ECH-associated protein 1a (Keap1a) and Keap1b gene expression in fish intestine (P < 0.05). These data indicated that deficient Folic Acid diet damaged fish intestinal antioxidant capacity partly by regulating Nrf2/Keap1 pathway. Additionally, Folic Acid Deficiency (0.1 mg kg(-1)) down-regulated claudin-b, claudin-c, claudin-3, occludin and zonula occludens 1 gene expression; whereas Folic Acid Deficiency (0.1 mg kg(-1)) up-regulated claudin-12, claudin-15, myosin light chain kinase (MLCK) and p38 mitogen activated protein kinase (p38 MAPK) gene expression in the PI, MI and DI (P < 0.05), suggesting that Folic Acid Deficiency may damage fish intestinal tight junctions associated with the mediation of MLCK and p38 MAPK gene expression. In conclusion, Folic Acid Deficiency (0.1 mg kg(-1)) impaired fish intestinal immunity, antioxidant capacity and tight junctions.

  • Immunity decreases, antioxidant system damages and tight junction changes in the intestine of grass carp (Ctenopharyngodon idella) during Folic Acid Deficiency: Regulation of NF-κB, Nrf2 and MLCK mRNA levels.
    Fish & Shellfish Immunology, 2016
    Co-Authors: Lei Shi, Lin Feng, Wei-dan Jiang, Yang Liu, Jun Jiang, Sheng-yao Kuang, Ling Tang, Wu-neng Tang, Yong-an Zhang
    Abstract:

    This investigation used the same growth trial as the previous study, which showed that Folic Acid Deficiency retarded growth in young grass carp (the percent weight gain of Groups 1-6 were 102.32 ± 3.41%, 137.25 ± 10.48%, 179.78 ± 3.95%, 164.33 ± 3.21%, 143.35 ± 8.12% and 115.28 ± 2.66%) [1]. In the present study, we investigated the effects of dietary Folic Acid on the immune response, antioxidant status and tight junctions in the intestine of young grass carp (Ctenopharyngodon idella). A total of 540 young grass carp were fed diets containing graded levels of Folic Acid at 0.10, 0.47, 1.03, 1.48, 1.88 and 3.12 mg kg(-1) diet for 8 weeks. The results indicated that Acid phosphatase and lysozyme activities, and the complement component 3 content in the proximal intestine (PI), mid intestine (MI) and distal intestine (DI) were decreased with Folic Acid Deficiency (0.1 mg kg(-1)) (P 

  • Folic Acid Deficiency impairs the gill health status associated with the NF-κB, MLCK and Nrf2 signaling pathways in the gills of young grass carp (Ctenopharyngodon idella).
    Fish & Shellfish Immunology, 2015
    Co-Authors: Lei Shi, Lin Feng, Wei-dan Jiang, Yang Liu, Jun Jiang, Juan Zhao, Sheng-yao Kuang, Ling Tang, Wu-neng Tang
    Abstract:

    The aim of this study was to investigate the effect of dietary Folic Acid on fish growth, the immune and barrier functions of fish gills, and the potential mechanisms of these effects. Young grass carp (Ctenophatyngodon idella) were fed diets containing graded levels of Folic Acid at 0.10 (basal diet), 0.47, 1.03, 1.48, 1.88 and 3.12 mg kg(-1) diet for 8 weeks. The results showed that Acid phosphatase and lysozyme activities and the complement component 3 content in fish gills decreased with Folic Acid Deficiency (P < 0.05). Folic Acid Deficiency up-regulated liver-expressed antimicrobial peptide 1, interleukin 1 beta, interleukin 8, tumor necrosis factor alpha, nuclear factor kappa B p65, I kappa B kinase alpha (IKK-alpha), IKK-beta and IKK-gamma gene expression. Folic Acid Deficiency down-regulated interleukin 10, transforming growth factor beta, I kappa B and target of rapamycin gene expression in fish gills (P < 0.05). These results showed that limited Folic Acid decreased fish gill immune status. Furthermore, Folic Acid Deficiency down-regulated claudin-b, claudin-c, claudin-3, occludin and zonula occludens 1 gene expression, whereas Folic Acid Deficiency up-regulated claudin-12, claudin-15, myosin light chain kinase and p38 mitogen activated protein kinase gene expression in fish gills (P < 0.05). These results suggested that Folic Acid Deficiency disrupted tight junction-mediated fish gill barrier function. Additionally, Folic Acid Deficiency increased the content of reactive oxygen species, protein carbonyl and malondialdehyde (MDA); Mn superoxide dismutase activity and gene expression; and Kelch-like-ECH-associated protein 1a (Keap1a) and Keap1b gene expression (P < 0.05). Conversely, Folic Acid Deficiency decreased Cu/Zn superoxide dismutase, catalase, glutathione peroxidase, glutathione s-transferases and glutathione reductase activities and gene expression as well as NF-E2-related factor 2 gene expression in fish gills (P < 0.05). All of these results indicated that Folic Acid Deficiency impaired fish gill health status via regulating gene expression of cytokines, tight junction proteins, antioxidant enzymes, NF-kappa B p65, MLCK and Nrf2. Based on percent weight gain, LZ activity and MDA content in the gills, the dietary Folic Acid requirements for young grass carp were 1.60, 2.07 and 2.08 mg kg(-1), respectively. (C) 2015 Published by Elsevier Ltd.

Yang Liu - One of the best experts on this subject based on the ideXlab platform.

  • immunity decreases antioxidant system damages and tight junction changes in the intestine of grass carp ctenopharyngodon idella during Folic Acid Deficiency regulation of nf κb nrf2 and mlck mrna levels
    Fish & Shellfish Immunology, 2016
    Co-Authors: Lei Shi, Lin Feng, Wei-dan Jiang, Yang Liu, Jun Jiang, Sheng-yao Kuang
    Abstract:

    This investigation used the same growth trial as the previous study, which showed that Folic Acid Deficiency retarded growth in young grass carp (the percent weight gain of Groups 1-6 were 102.32 ± 3.41%, 137.25 ± 10.48%, 179.78 ± 3.95%, 164.33 ± 3.21%, 143.35 ± 8.12% and 115.28 ± 2.66%) [1]. In the present study, we investigated the effects of dietary Folic Acid on the immune response, antioxidant status and tight junctions in the intestine of young grass carp (Ctenopharyngodon idella). A total of 540 young grass carp were fed diets containing graded levels of Folic Acid at 0.10, 0.47, 1.03, 1.48, 1.88 and 3.12 mg kg(-1) diet for 8 weeks. The results indicated that Acid phosphatase and lysozyme activities, and the complement component 3 content in the proximal intestine (PI), mid intestine (MI) and distal intestine (DI) were decreased with Folic Acid Deficiency (0.1 mg kg(-1)) (P < 0.05). Folic Acid Deficiency (0.1 mg kg(-1)) up-regulated interleukin 1β, interleukin 8, tumor necrosis factor α, nuclear factor κB p65 (NF-κB p65), IκB kinase α (IKK-α), IKK-β and IKK-γ gene expression, meanwhile down-regulated interleukin 10, transforming growth factor β, IκB and target of rapamycin gene expression in the PI, MI and DI (P < 0.05). These data suggested that Folic Acid Deficiency decreased fish intestinal innate immune function may be partly contributed to the regulation of NF-κB p65 pathway. Moreover, the activities and corresponding gene expression of glutathione content, Cu/Zn superoxide dismutase, catalase, glutathione peroxidase, glutathione s-transferases and glutathione reductase in fish intestine were depressed by deficient Folic Acid diet (0.1 mg kg(-1)) (P < 0.05). Furthermore, Folic Acid Deficiency (0.1 mg kg(-1)) down-regulated NF-E2-related factor 2 (Nrf2) gene expression, up-regulated Kelch-like-ECH-associated protein 1a (Keap1a) and Keap1b gene expression in fish intestine (P < 0.05). These data indicated that deficient Folic Acid diet damaged fish intestinal antioxidant capacity partly by regulating Nrf2/Keap1 pathway. Additionally, Folic Acid Deficiency (0.1 mg kg(-1)) down-regulated claudin-b, claudin-c, claudin-3, occludin and zonula occludens 1 gene expression; whereas Folic Acid Deficiency (0.1 mg kg(-1)) up-regulated claudin-12, claudin-15, myosin light chain kinase (MLCK) and p38 mitogen activated protein kinase (p38 MAPK) gene expression in the PI, MI and DI (P < 0.05), suggesting that Folic Acid Deficiency may damage fish intestinal tight junctions associated with the mediation of MLCK and p38 MAPK gene expression. In conclusion, Folic Acid Deficiency (0.1 mg kg(-1)) impaired fish intestinal immunity, antioxidant capacity and tight junctions.

  • Immunity decreases, antioxidant system damages and tight junction changes in the intestine of grass carp (Ctenopharyngodon idella) during Folic Acid Deficiency: Regulation of NF-κB, Nrf2 and MLCK mRNA levels.
    Fish & Shellfish Immunology, 2016
    Co-Authors: Lei Shi, Lin Feng, Wei-dan Jiang, Yang Liu, Jun Jiang, Sheng-yao Kuang, Ling Tang, Wu-neng Tang, Yong-an Zhang
    Abstract:

    This investigation used the same growth trial as the previous study, which showed that Folic Acid Deficiency retarded growth in young grass carp (the percent weight gain of Groups 1-6 were 102.32 ± 3.41%, 137.25 ± 10.48%, 179.78 ± 3.95%, 164.33 ± 3.21%, 143.35 ± 8.12% and 115.28 ± 2.66%) [1]. In the present study, we investigated the effects of dietary Folic Acid on the immune response, antioxidant status and tight junctions in the intestine of young grass carp (Ctenopharyngodon idella). A total of 540 young grass carp were fed diets containing graded levels of Folic Acid at 0.10, 0.47, 1.03, 1.48, 1.88 and 3.12 mg kg(-1) diet for 8 weeks. The results indicated that Acid phosphatase and lysozyme activities, and the complement component 3 content in the proximal intestine (PI), mid intestine (MI) and distal intestine (DI) were decreased with Folic Acid Deficiency (0.1 mg kg(-1)) (P 

  • Folic Acid Deficiency impairs the gill health status associated with the NF-κB, MLCK and Nrf2 signaling pathways in the gills of young grass carp (Ctenopharyngodon idella).
    Fish & Shellfish Immunology, 2015
    Co-Authors: Lei Shi, Lin Feng, Wei-dan Jiang, Yang Liu, Jun Jiang, Juan Zhao, Sheng-yao Kuang, Ling Tang, Wu-neng Tang
    Abstract:

    The aim of this study was to investigate the effect of dietary Folic Acid on fish growth, the immune and barrier functions of fish gills, and the potential mechanisms of these effects. Young grass carp (Ctenophatyngodon idella) were fed diets containing graded levels of Folic Acid at 0.10 (basal diet), 0.47, 1.03, 1.48, 1.88 and 3.12 mg kg(-1) diet for 8 weeks. The results showed that Acid phosphatase and lysozyme activities and the complement component 3 content in fish gills decreased with Folic Acid Deficiency (P < 0.05). Folic Acid Deficiency up-regulated liver-expressed antimicrobial peptide 1, interleukin 1 beta, interleukin 8, tumor necrosis factor alpha, nuclear factor kappa B p65, I kappa B kinase alpha (IKK-alpha), IKK-beta and IKK-gamma gene expression. Folic Acid Deficiency down-regulated interleukin 10, transforming growth factor beta, I kappa B and target of rapamycin gene expression in fish gills (P < 0.05). These results showed that limited Folic Acid decreased fish gill immune status. Furthermore, Folic Acid Deficiency down-regulated claudin-b, claudin-c, claudin-3, occludin and zonula occludens 1 gene expression, whereas Folic Acid Deficiency up-regulated claudin-12, claudin-15, myosin light chain kinase and p38 mitogen activated protein kinase gene expression in fish gills (P < 0.05). These results suggested that Folic Acid Deficiency disrupted tight junction-mediated fish gill barrier function. Additionally, Folic Acid Deficiency increased the content of reactive oxygen species, protein carbonyl and malondialdehyde (MDA); Mn superoxide dismutase activity and gene expression; and Kelch-like-ECH-associated protein 1a (Keap1a) and Keap1b gene expression (P < 0.05). Conversely, Folic Acid Deficiency decreased Cu/Zn superoxide dismutase, catalase, glutathione peroxidase, glutathione s-transferases and glutathione reductase activities and gene expression as well as NF-E2-related factor 2 gene expression in fish gills (P < 0.05). All of these results indicated that Folic Acid Deficiency impaired fish gill health status via regulating gene expression of cytokines, tight junction proteins, antioxidant enzymes, NF-kappa B p65, MLCK and Nrf2. Based on percent weight gain, LZ activity and MDA content in the gills, the dietary Folic Acid requirements for young grass carp were 1.60, 2.07 and 2.08 mg kg(-1), respectively. (C) 2015 Published by Elsevier Ltd.