Oxidative Stress Markers in Vitamin B12 Deficiency

In this study, we report the status of oxidative stress markers in vitamin B12 deficiency and their relation to clinical, laboratory, and neurophysiological findings. Fifty-one subjects with serum vitamin B12 deficiency (<211 pg/ml) were included. Plasma glutathione (GSH), malondialdehyde (MDA) a...

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Published inMolecular neurobiology Vol. 54; no. 2; pp. 1278 - 1284
Main Authors Misra, Usha Kant, Kalita, Jayantee, Singh, Sandeep Kumar, Rahi, Sushil Kumar
Format Journal Article
LanguageEnglish
Published New York Springer US 01.03.2017
Springer Nature B.V
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Online AccessGet full text
ISSN0893-7648
1559-1182
1559-1182
DOI10.1007/s12035-016-9736-2

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Abstract In this study, we report the status of oxidative stress markers in vitamin B12 deficiency and their relation to clinical, laboratory, and neurophysiological findings. Fifty-one subjects with serum vitamin B12 deficiency (<211 pg/ml) were included. Plasma glutathione (GSH), malondialdehyde (MDA) and serum total antioxidant capacity (TAC) were measured in the patients and 53 controls. These markers were also compared between subacute combined degeneration (SACD) and non-SACD vitamin B12 deficiency patients groups as well as with normal controls. In the patients, GSH, MDA and TAC were correlated with demographic, clinical, hematological, biochemical, nerve conduction study (NCS), visual evoked potential (VEP) and somatosensory-evoked potential (SEP) findings. In the study group, 20 (39.2 %) patients had SACD manifesting with myeloneuropathy, cognitive or behavioral abnormalities, and 31(60.8 %) patients had non-SACD neurological manifestations. The GSH (2.46 ± 0.32 vs. 2.70 ± 0.36 mg/dl; P  = 0.002) and TAC (2.13 ± 0.38 vs. 2.33 ± 0.24 nmol Trolox eq/l, P  = 0.005) levels were lower, and MDA levels (4.01 ± 0.69 vs. 3.00 ± 0.45 nmol/ml, P  < 0.001) were higher in B12 deficiency group compared with controls. Similar trend was found in SACD and non-SACD vitamin B12 deficiency groups. GSH levels correlated with abnormal VEP ( r  = 0.54; P  < 0.01), TAC with female gender ( r  = 0.43; P  = 0.002) and joint position impairment ( r  = −0.34; P  = 0.01), and MDA with LDH ( r  = 0.41; P  = 0.01). Vitamin B12 deficiency was associated with reduction in GSH and TAC and increase in MDA levels which were more marked in SACD compared to non-SACD group.
AbstractList In this study, we report the status of oxidative stress markers in vitamin B12 deficiency and their relation to clinical, laboratory, and neurophysiological findings. Fifty-one subjects with serum vitamin B12 deficiency (<211 pg/ml) were included. Plasma glutathione (GSH), malondialdehyde (MDA) and serum total antioxidant capacity (TAC) were measured in the patients and 53 controls. These markers were also compared between subacute combined degeneration (SACD) and non-SACD vitamin B12 deficiency patients groups as well as with normal controls. In the patients, GSH, MDA and TAC were correlated with demographic, clinical, hematological, biochemical, nerve conduction study (NCS), visual evoked potential (VEP) and somatosensory-evoked potential (SEP) findings. In the study group, 20 (39.2 %) patients had SACD manifesting with myeloneuropathy, cognitive or behavioral abnormalities, and 31(60.8 %) patients had non-SACD neurological manifestations. The GSH (2.46 ± 0.32 vs. 2.70 ± 0.36 mg/dl; P = 0.002) and TAC (2.13 ± 0.38 vs. 2.33 ± 0.24 nmol Trolox eq/l, P = 0.005) levels were lower, and MDA levels (4.01 ± 0.69 vs. 3.00 ± 0.45 nmol/ml, P < 0.001) were higher in B12 deficiency group compared with controls. Similar trend was found in SACD and non-SACD vitamin B12 deficiency groups. GSH levels correlated with abnormal VEP (r = 0.54; P < 0.01), TAC with female gender (r = 0.43; P = 0.002) and joint position impairment (r = -0.34; P = 0.01), and MDA with LDH (r = 0.41; P = 0.01). Vitamin B12 deficiency was associated with reduction in GSH and TAC and increase in MDA levels which were more marked in SACD compared to non-SACD group.
In this study, we report the status of oxidative stress markers in vitamin B12 deficiency and their relation to clinical, laboratory, and neurophysiological findings. Fifty-one subjects with serum vitamin B12 deficiency (<211 pg/ml) were included. Plasma glutathione (GSH), malondialdehyde (MDA) and serum total antioxidant capacity (TAC) were measured in the patients and 53 controls. These markers were also compared between subacute combined degeneration (SACD) and non-SACD vitamin B12 deficiency patients groups as well as with normal controls. In the patients, GSH, MDA and TAC were correlated with demographic, clinical, hematological, biochemical, nerve conduction study (NCS), visual evoked potential (VEP) and somatosensory-evoked potential (SEP) findings. In the study group, 20 (39.2 %) patients had SACD manifesting with myeloneuropathy, cognitive or behavioral abnormalities, and 31(60.8 %) patients had non-SACD neurological manifestations. The GSH (2.46 plus or minus 0.32 vs. 2.70 plus or minus 0.36 mg/dl; P=0.002) and TAC (2.13 plus or minus 0.38 vs. 2.33 plus or minus 0.24 nmol Trolox eq/l, P=0.005) levels were lower, and MDA levels (4.01 plus or minus 0.69 vs. 3.00 plus or minus 0.45 nmol/ml, P<0.001) were higher in B12 deficiency group compared with controls. Similar trend was found in SACD and non-SACD vitamin B12 deficiency groups. GSH levels correlated with abnormal VEP (r=0.54; P<0.01), TAC with female gender (r=0.43; P=0.002) and joint position impairment (r=-0.34; P=0.01), and MDA with LDH (r=0.41; P=0.01). Vitamin B12 deficiency was associated with reduction in GSH and TAC and increase in MDA levels which were more marked in SACD compared to non-SACD group.
In this study, we report the status of oxidative stress markers in vitamin B12 deficiency and their relation to clinical, laboratory, and neurophysiological findings. Fifty-one subjects with serum vitamin B12 deficiency (<211 pg/ml) were included. Plasma glutathione (GSH), malondialdehyde (MDA) and serum total antioxidant capacity (TAC) were measured in the patients and 53 controls. These markers were also compared between subacute combined degeneration (SACD) and non-SACD vitamin B12 deficiency patients groups as well as with normal controls. In the patients, GSH, MDA and TAC were correlated with demographic, clinical, hematological, biochemical, nerve conduction study (NCS), visual evoked potential (VEP) and somatosensory-evoked potential (SEP) findings. In the study group, 20 (39.2 %) patients had SACD manifesting with myeloneuropathy, cognitive or behavioral abnormalities, and 31(60.8 %) patients had non-SACD neurological manifestations. The GSH (2.46 ± 0.32 vs. 2.70 ± 0.36 mg/dl; P  = 0.002) and TAC (2.13 ± 0.38 vs. 2.33 ± 0.24 nmol Trolox eq/l, P  = 0.005) levels were lower, and MDA levels (4.01 ± 0.69 vs. 3.00 ± 0.45 nmol/ml, P  < 0.001) were higher in B12 deficiency group compared with controls. Similar trend was found in SACD and non-SACD vitamin B12 deficiency groups. GSH levels correlated with abnormal VEP ( r  = 0.54; P  < 0.01), TAC with female gender ( r  = 0.43; P  = 0.002) and joint position impairment ( r  = −0.34; P  = 0.01), and MDA with LDH ( r  = 0.41; P  = 0.01). Vitamin B12 deficiency was associated with reduction in GSH and TAC and increase in MDA levels which were more marked in SACD compared to non-SACD group.
In this study, we report the status of Oxidative Stress Markers in Vitamin B12 Deficiency and their relation to clinical, laboratory, and neurophysiological findings. Fifty-one subjects with serum vitamin B12 deficiency (<211 pg/ml) were included. Plasma glutathione (GSH), malondialdehyde (MDA) and serum total antioxidant capacity (TAC) were measured in the patients and 53 controls. These markers were also compared between subacute combined degeneration (SACD) and non-SACD vitamin B12 deficiency patients groups as well as with normal controls. In the patients, GSH, MDA and TAC were correlated with demographic, clinical, hematological, biochemical, nerve conduction study (NCS), visual evoked potential (VEP) and somatosensory-evoked potential (SEP) findings. In the study group, 20 (39.2 %) patients had SACD manifesting with myeloneuropathy, cognitive or behavioral abnormalities, and 31(60.8 %) patients had non-SACD neurological manifestations. The GSH (2.46±0.32 vs. 2.70±0.36 mg/dl; P=0.002) and TAC (2.13±0.38 vs. 2.33±0.24 nmol Trolox eq/l, P=0.005) levels were lower, and MDA levels (4.01±0.69 vs. 3.00±0.45 nmol/ml, P<0.001) were higher in B12 deficiency group compared with controls. Similar trend was found in SACD and non-SACD vitamin B12 deficiency groups. GSH levels correlated with abnormal VEP (r=0.54; P<0.01), TAC with female gender (r=0.43; P=0.002) and joint position impairment (r=-0.34; P=0.01), and MDA with LDH (r=0.41; P=0.01). Vitamin B12 deficiency was associated with reduction in GSH and TAC and increase in MDA levels which were more marked in SACD compared to non-SACD group.
In this study, we report the status of oxidative stress markers in vitamin B12 deficiency and their relation to clinical, laboratory, and neurophysiological findings. Fifty-one subjects with serum vitamin B12 deficiency (<211 pg/ml) were included. Plasma glutathione (GSH), malondialdehyde (MDA) and serum total antioxidant capacity (TAC) were measured in the patients and 53 controls. These markers were also compared between subacute combined degeneration (SACD) and non-SACD vitamin B12 deficiency patients groups as well as with normal controls. In the patients, GSH, MDA and TAC were correlated with demographic, clinical, hematological, biochemical, nerve conduction study (NCS), visual evoked potential (VEP) and somatosensory-evoked potential (SEP) findings. In the study group, 20 (39.2 %) patients had SACD manifesting with myeloneuropathy, cognitive or behavioral abnormalities, and 31(60.8 %) patients had non-SACD neurological manifestations. The GSH (2.46 ± 0.32 vs. 2.70 ± 0.36 mg/dl; P = 0.002) and TAC (2.13 ± 0.38 vs. 2.33 ± 0.24 nmol Trolox eq/l, P = 0.005) levels were lower, and MDA levels (4.01 ± 0.69 vs. 3.00 ± 0.45 nmol/ml, P < 0.001) were higher in B12 deficiency group compared with controls. Similar trend was found in SACD and non-SACD vitamin B12 deficiency groups. GSH levels correlated with abnormal VEP (r = 0.54; P < 0.01), TAC with female gender (r = 0.43; P = 0.002) and joint position impairment (r = -0.34; P = 0.01), and MDA with LDH (r = 0.41; P = 0.01). Vitamin B12 deficiency was associated with reduction in GSH and TAC and increase in MDA levels which were more marked in SACD compared to non-SACD group.In this study, we report the status of oxidative stress markers in vitamin B12 deficiency and their relation to clinical, laboratory, and neurophysiological findings. Fifty-one subjects with serum vitamin B12 deficiency (<211 pg/ml) were included. Plasma glutathione (GSH), malondialdehyde (MDA) and serum total antioxidant capacity (TAC) were measured in the patients and 53 controls. These markers were also compared between subacute combined degeneration (SACD) and non-SACD vitamin B12 deficiency patients groups as well as with normal controls. In the patients, GSH, MDA and TAC were correlated with demographic, clinical, hematological, biochemical, nerve conduction study (NCS), visual evoked potential (VEP) and somatosensory-evoked potential (SEP) findings. In the study group, 20 (39.2 %) patients had SACD manifesting with myeloneuropathy, cognitive or behavioral abnormalities, and 31(60.8 %) patients had non-SACD neurological manifestations. The GSH (2.46 ± 0.32 vs. 2.70 ± 0.36 mg/dl; P = 0.002) and TAC (2.13 ± 0.38 vs. 2.33 ± 0.24 nmol Trolox eq/l, P = 0.005) levels were lower, and MDA levels (4.01 ± 0.69 vs. 3.00 ± 0.45 nmol/ml, P < 0.001) were higher in B12 deficiency group compared with controls. Similar trend was found in SACD and non-SACD vitamin B12 deficiency groups. GSH levels correlated with abnormal VEP (r = 0.54; P < 0.01), TAC with female gender (r = 0.43; P = 0.002) and joint position impairment (r = -0.34; P = 0.01), and MDA with LDH (r = 0.41; P = 0.01). Vitamin B12 deficiency was associated with reduction in GSH and TAC and increase in MDA levels which were more marked in SACD compared to non-SACD group.
Author Misra, Usha Kant
Rahi, Sushil Kumar
Kalita, Jayantee
Singh, Sandeep Kumar
Author_xml – sequence: 1
  givenname: Usha Kant
  surname: Misra
  fullname: Misra, Usha Kant
  email: drukmisra@rediffmail.com
  organization: Department of Neurology, Sanjay Gandhi Post Graduate Institute of Medical Sciences
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  givenname: Jayantee
  surname: Kalita
  fullname: Kalita, Jayantee
  organization: Department of Neurology, Sanjay Gandhi Post Graduate Institute of Medical Sciences
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  givenname: Sandeep Kumar
  surname: Singh
  fullname: Singh, Sandeep Kumar
  organization: Department of Neurology, Sanjay Gandhi Post Graduate Institute of Medical Sciences
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  givenname: Sushil Kumar
  surname: Rahi
  fullname: Rahi, Sushil Kumar
  organization: Department of Neurology, Sanjay Gandhi Post Graduate Institute of Medical Sciences
BackLink https://www.ncbi.nlm.nih.gov/pubmed/26843105$$D View this record in MEDLINE/PubMed
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Molecular Neurobiology is a copyright of Springer, 2017.
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Fri Jul 25 09:48:33 EDT 2025
Thu Apr 03 06:58:58 EDT 2025
Tue Jul 01 01:04:35 EDT 2025
Thu Apr 24 23:05:30 EDT 2025
Fri Feb 21 02:38:07 EST 2025
IsPeerReviewed true
IsScholarly true
Issue 2
Keywords Nerve conduction study
Oxidative stress
Total antioxidant capacity
Visual evoked potential
Subacute combined degeneration
Vitamin B12
Malondialdehyde
Glutathione
Language English
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Springer Nature B.V
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SSID ssj0022107
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Snippet In this study, we report the status of oxidative stress markers in vitamin B12 deficiency and their relation to clinical, laboratory, and neurophysiological...
In this study, we report the status of Oxidative Stress Markers in Vitamin B12 Deficiency and their relation to clinical, laboratory, and neurophysiological...
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springer
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StartPage 1278
SubjectTerms Adult
Antioxidants
Biomarkers - metabolism
Biomedical and Life Sciences
Biomedicine
Cell Biology
Female
Glutathione - metabolism
Humans
Male
Malondialdehyde - metabolism
Middle Aged
Neural Conduction - physiology
Neurobiology
Neurology
Neurons
Neurosciences
Oxidative stress
Oxidative Stress - physiology
Vitamin B
Vitamin B 12 Deficiency - diagnosis
Vitamin B 12 Deficiency - metabolism
Vitamin deficiency
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Title Oxidative Stress Markers in Vitamin B12 Deficiency
URI https://link.springer.com/article/10.1007/s12035-016-9736-2
https://www.ncbi.nlm.nih.gov/pubmed/26843105
https://www.proquest.com/docview/1868545108
https://www.proquest.com/docview/1826658414
https://www.proquest.com/docview/1877836585
Volume 54
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