scholarly journals Combined glyoxalase 1 dysfunction and vitamin B6 deficiency in a schizophrenia model system causes mitochondrial dysfunction in the prefrontal cortex

Redox Biology ◽  
2021 ◽  
pp. 102057
Author(s):  
Kazuya Toriumi ◽  
Stefano Berto ◽  
Shin Koike ◽  
Noriyoshi Usui ◽  
Takashi Dan ◽  
...  
Author(s):  
V.J. Montpetit ◽  
S. Dancea ◽  
L. Tryphonas ◽  
D.F. Clapin

Very large doses of pyridoxine (vitamin B6) are neurotoxic in humans, selectively affecting the peripheral sensory nerves. We have undertaken a study of the morphological and biochemical aspects of pyridoxine neurotoxicity in an animal model system. Early morphological changes in dorsal root ganglia (DRG) associated with pyridoxine megadoses include proliferation of neurofilaments, ribosomes, rough endoplasmic reticulum, and Golgi complexes. We present in this report evidence of the formation of unique aggregates of microtubules and membranes in the proximal processes of DRG which are induced by high levels of pyridoxine.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Ashley M. Fields ◽  
Kevin Welle ◽  
Elaine S. Ho ◽  
Clementina Mesaros ◽  
Martha Susiarjo

AbstractIn pancreatic islets, catabolism of tryptophan into serotonin and serotonin receptor 2B (HTR2B) activation is crucial for β-cell proliferation and maternal glucose regulation during pregnancy. Factors that reduce serotonin synthesis and perturb HTR2B signaling are associated with decreased β-cell number, impaired insulin secretion, and gestational glucose intolerance in mice. Albeit the tryptophan-serotonin pathway is dependent on vitamin B6 bioavailability, how vitamin B6 deficiency impacts β-cell proliferation during pregnancy has not been investigated. In this study, we created a vitamin B6 deficient mouse model and investigated how gestational deficiency influences maternal glucose tolerance. Our studies show that gestational vitamin B6 deficiency decreases serotonin levels in maternal pancreatic islets and reduces β-cell proliferation in an HTR2B-dependent manner. These changes were associated with glucose intolerance and insulin resistance, however insulin secretion remained intact. Our findings suggest that vitamin B6 deficiency-induced gestational glucose intolerance involves additional mechanisms that are complex and insulin independent.


1980 ◽  
Vol 170 (4) ◽  
pp. 376-387 ◽  
Author(s):  
U.N. Riede ◽  
W. Sandritter ◽  
A. Pietzsch ◽  
R. Rohrbach

1998 ◽  
Vol 217 (1) ◽  
pp. 97-103 ◽  
Author(s):  
P. G. Masse ◽  
I. Ziv ◽  
D. E. C. Cole ◽  
J. D. Mahuren ◽  
S. M. Donovan ◽  
...  

1994 ◽  
Vol 50 (2) ◽  
pp. 127-129 ◽  
Author(s):  
T. Oka ◽  
N. Komori ◽  
M. Kuwahata ◽  
I. Suzuki ◽  
M. Okada ◽  
...  

1990 ◽  
Vol 587 (1) ◽  
pp. 292-293
Author(s):  
D. S. KELLEY ◽  
M. C. SCHAEFFER ◽  
D. A. SAMPSON ◽  
P. C. TAYLOR ◽  
Y. M. RIVERA

2009 ◽  
Vol 23 (1) ◽  
pp. 43-49 ◽  
Author(s):  
Irene Mackraj ◽  
Govender Thirumala ◽  
Premjith Gathiram

1939 ◽  
Vol 42 (1) ◽  
pp. 180-182 ◽  
Author(s):  
T. H. Jukes

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