Thiamine deficiency and recovery: impact of recurrent episodes and beneficial effect of treatment with Trolox and dimethyl sulfoxide

Gomes, Ketren Carvalho; Lima, Francisco Wanderson Bizerra; Aguiar, Helen Quézia da Silva; Araújo, Suiane Silva de; Cordova, Clarissa Amorim Silva de; Córdova, Fabiano Mendes de

doi:10.1007/s00210-021-02148-5

Cited by 1 publication

(11 citation statements)

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“…The injected volumes in both protocols were adjusted to 0.1 ml/10 g of body weight. 5,23 The control groups received AIN-93M standard chow (6.0 mg thiamine hydrochloride per kilogram of feed; PRAG Soluc¸ões Biocieˆncias) according to the American Institute of Nutrition 24 ad libitum throughout the treatments. The deficient groups received thiamine-deficient AIN-93TD chow (0.0 mg thiamine hydrochloride per kilogram of feed; PRAG Soluc¸ões Biocieˆncias) during periods of deficiency induction.…”

Section: Treatmentsmentioning

confidence: 99%

“…The deficient groups received thiamine-deficient AIN-93TD chow (0.0 mg thiamine hydrochloride per kilogram of feed; PRAG Soluc¸ões Biocieˆncias) during periods of deficiency induction. 5,6,12 The constituents of the thiamine-deficient diet were identical to those of the standard diet, except for a lack of vitamins.…”

Section: Treatmentsmentioning

confidence: 99%

“…23 Proteins were transferred to nitrocellulose membranes (1.2 mA/cm 2 ; 1.5 h) using a wet blotting apparatus (WEST-i10 TM , Loccus). 5 The membranes were blocked for 1 h with 2% BSA in Tris buffered saline (TBS; 10 mM Tris, 150 mM NaCl, pH 7.5). ERK1/2 total and phosphorylated forms, as well as b-actin, were detected by overnight incubation with specific antibodies diluted at 1:10,000 (P-ERK1/2 and b-actin) or 1:40,000 (T-ERK1/2) in TBS-T (10 mM Tris, 150 mM NaCl, 0.1% Tween V R 20, pH 7.5) containing 2.5% BSA.…”

Section: Western Blottingmentioning

confidence: 99%

“…ROS, tumor necrosis factor and interleukins are related to the activation of mitogenactivated protein kinase (MAPK) pathways, 4 such as p38MAPK and extracellular signal-regulated kinases 1 and 2 (ERK1/2), suggesting the involvement of these signaling pathways in the pathogenesis of thiamine deficiency-induced neurodegeneration. 5,6 Experimental thiamine deficiency models for in vivo studies in laboratory animals allow for in-depth investigation of the anatomical, physiological and cellular basis of the neurological disorders that occur in this deficiency. Two well-established experimental models for rodents are used to study thiamine deficiency.…”

Section: Introductionmentioning

confidence: 99%

“…For this, we evaluated the modulation of ERK1/2 phosphorylation in the nervous tissue as a parameter, as it is an important signaling pathway for several cellular functions and is sensitive to several stress factors, including thiamine deficiency. 5…”

Section: Introductionmentioning

confidence: 99%

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ERK1/2 modulation in the central nervous system of male and female thiamine-deficient mice with amprolium

da Silva,

Lima,

Moura

et al. 2023

Lab Anim

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Thiamine deficiency experimental models focus on using the pyrithiamine analog in male rodents, making the thiamine deficiency effects in females and the use of other thiamine antagonists, such as amprolium, unknown. We investigated the impact of thiamine deficiency with amprolium in the cerebral cortex and thalamus of male and female mice by evaluating the modulation of ERK1/2 phosphorylation. The animals were exposed for 20 days to thiamine-deficient chow with different doses of amprolium (20, 40, 60 and 80 mg/kg) and at different treatment periods (five, 10, 15 or 20 days) at a dose of 60 mg/kg. After treatments, ERK1/2 phosphorylation was analyzed by western blot. In male mice, we observed a progressive increase in ERK1/2 phosphorylation in both the cerebral cortex and thalamus in response to the dose of amprolium. In females, ERK1/2 phosphorylation did not progressively increase in response to the amprolium dosage. However, an increase in phosphorylation at the higher doses of 60 and 80 mg/kg was observed. We observed a more intense increase in ERK1/2 phosphorylation in males’ cerebral cortex and thalamus from 10 days onwards. In females, the ERK1/2 modulation profiles were similar. The results show that thiamine deficiency induction with amprolium is efficient, compatible with other recognized models that use pyrithiamine, showing changes in cell signaling in the nervous system. The study showed differences in response to thiamine deficiency with amprolium between male and female mice in relation to ERK1/2 phosphorylation and demonstrated that females respond positively to the method and can also be used as model animals.

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Section: Treatmentsmentioning

confidence: 99%

Section: Treatmentsmentioning

confidence: 99%