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 in | Molecular neurobiology Vol. 54; no. 2; pp. 1278 - 1284 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
New York
Springer US
01.03.2017
Springer Nature B.V |
Subjects | |
Online Access | Get full text |
ISSN | 0893-7648 1559-1182 1559-1182 |
DOI | 10.1007/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 – sequence: 2 givenname: Jayantee surname: Kalita fullname: Kalita, Jayantee organization: Department of Neurology, Sanjay Gandhi Post Graduate Institute of Medical Sciences – sequence: 3 givenname: Sandeep Kumar surname: Singh fullname: Singh, Sandeep Kumar organization: Department of Neurology, Sanjay Gandhi Post Graduate Institute of Medical Sciences – sequence: 4 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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Keywords | Nerve conduction study Oxidative stress Total antioxidant capacity Visual evoked potential Subacute combined degeneration Vitamin B12 Malondialdehyde Glutathione |
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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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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 |
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