Distribution and Utilization of Vitamin E in Different Organs of Wild Bats from Different Food Groups.

In this work, we examined the levels of vitamin E in the heart, liver, and kidneys of four species of adult male bats with distinct feeding habits. Our results indicate consistent vitamin E levels in the heart across all four bat species, suggesting the presence of regulatory mechanisms. Additionally, the liver displayed notably higher vitamin E levels in nectarivorous and frugivorous bats, while hematophagous bats exhibited lower levels, indicating a link between dietary intake and liver vitamin E levels. Furthermore, correlation analysis provided additional insights into the relationships between vitamin E and key antioxidant parameters in the livers of bats. On the other hand, no correlation was observed between vitamin E and key antioxidant parameters in the heart. Intriguingly, vitamin E was not detected in the kidneys, likely due to physiological factors and the prioritization of vitamin E mobilization in the heart, where it serves critical physiological functions. This unexpected absence of vitamin E in bat kidneys highlights the unique metabolic demands and prioritization of vitamin mobilization in wild animals like bats, compared to conventional animal models. These findings provide insight into the intricate distribution and utilization of vitamin E in bats, emphasizing the influence of dietary intake and metabolic adaptations on vitamin E levels in different organs.

The effects of α-tocopherol administration in chronically lead exposed workers.

The aim of the study was to investigate whether α-tocopherol supplementation for workers who are chronically exposed to lead would normalize/improve the values of parameters that are associated with the lead-induced oxidative stress. Study population included chronically lead exposed males who were divided into two groups. Workers in the first group (reference group) were not given any antioxidants, while workers in the second group (αT group) received supplementation with α-tocopherol. After treatment, the blood lead and leukocyte malondialdehyde levels decreased significantly in the αT group compared to the baseline levels and reference group. However, the erythrocyte malondialdehyde, conjugated dienes, and lipofuscin levels significantly increased compared to the baseline levels. The glutathione level significantly increased compared with the baseline. Effects of supplementation with α-tocopherol on oxidative damage were not satisfactory. Therefore, there is no reason to administer α-tocopherol to workers chronically exposed to lead as a prophylaxis of lead poisoning.

Combination Therapy with Losartan and α-Tocopherol in Acute Ureteral Obstruction-Induced Renal Excretory Dysfunction and Acidification Defect.

BACKGROUND: Previous study by the authors showed that a-tocopherol prevents oxidative stress but would not improve depressed excretory variables in post-obstructed kidney (POK) after release of 24-h unilateral ureteral obstruction (UUO). This study is a supplementary investigation on the effects of a-tocopherol combined with an antagonist of angiotensin-II type-1 (AT1) receptor on renal dysfunction following release of acute UUO. METHODS: The left ureter was ligated in different groups of male Sprague-Dawley rats that received normal saline, losartan or losartan/a-tocopherol (n=6 in each group). After releasing 24-h UUO, urine of each kidney was separately collected under paraffin during 1-3 h of post-release period and then both kidneys were removed for measuring malondialdehyde (MDA) and ferric reducing/antioxidant power (FRAP). RESULTS: Losartan-treatment decreased MDA and increased FRAP, creatinine-clearance and sodium-reabsorption in POK, while co-treatment with losartan and a-tocopherol not only augmented improvement in these variables but also elevated potassium-excretion, free-water reabsorption and urine-osmolality. However, UUO-induced fall in urinary pCO2 and rise in pH and bicarbonate-excretion of POK were ameliorated equally with losartan and losartan/a-tocopherol. CONCLUSION: Activation of AT1-receptor contributes to the development of renal distal acidification defect induced by acute ureteral obstruction. The co-treatment with losartan and a-tocopherol showed that their effects on preventing oxidative stress along with ameliorating glomerular filtration and tubular fluid-delivery in POK could lead to improvement in tubular transport of sodium and potassium as well as urine-concentrating ability at the early post-release period.

Hallazgos clínicos y moleculares en una paciente con ataxia por deficiencia de vitamina E, homocigota para la mutación c.205-1G>C en el gen TTPA / Clinical and molecular findings in a patient with ataxia with vitamin E deficiency, homozygous for the c.205-1G>C mutation in the TTPA gene

Introducción. La ataxia por deficiencia de vitamina E es causada por mutaciones en el gen TTPA . Está caracterizada por ataxia, arreflexia, temblor cefálico, pérdida de la propiocepción, Babinsky, disdiadococinesia, retinitis pigmentosa y cardiomiopatía. Caso clínico. Se trató de una paciente del sexo femenino de 11 años, padres consanguíneos, valorada por dolor y parestesias en miembros inferiores, disartria y problemas para escribir y masticar. El examen físico mostró fuerza distal disminuida, hiperreflexia, Babinsky, disminución en la propiocepción, pie cavo bilateral, dismetría, disdiadococinesia y Romberg positivo. El estudio para ataxia de Friedreich resultó normal, aunque presentó bajos niveles de a-tocoferol y se identificó una mutación homocigota c.205-1G>C en el gen TTPA . Se inició tratamiento con vitamina E con lo que mostró mejoría. Conclusiones. Ante la presencia de manifestaciones parecidas a la ataxia de Friedreich se sugiere evaluar niveles plasmáticos de α-tocoferol y realizar estudios genéticos confirmatorios. El tratamiento con vitamina E disminuye los síntomas en los afectados y los presintomáticos no desarrollan manifestaciones del trastorno. Se han reportado pocos casos en Latinoamérica. En esta paciente se encontró una mutación en estado homocigoto fuera de las áreas de mayor prevalencia. Dichos hallazgos clínicos pueden indicar que la mutación c.205-1G>C se asocia con un cuadro severo.

Background. Ataxia with vitamin E deficiency is a disorder caused by mutations in the TTPA gene. Common symptoms include ataxia, areflexia, head titubation, loss of proprioception, Babinsky sign, dysdiadochokinesia, pigmentary retinopathy and cardiomyopathy. Case report. The patient was the first child of consanguineous parents. She presented at 10 years of age due to bilateral lower limb pain and numbness and difficulty in speech, writing and chewing. Physical examination showed dysarthria, diminished distal strength, hyperreflexia, positive Babinsky sign, decreased proprioception, pes cavus, dysmetria, dysdiadochokinesia and positive Romberg sign. Genetic screening for the Friedreich's ataxia gene resulted negative, α-tocopherol levels were low and TTPA gene sequentiation detected the homozygous mutation c.205-1G >C in intron 1. Treatment was initiated with vitamin E, showing improvement of symptoms. Conclusions. The presence of Friedreich's ataxia-like phenotype suggests the need to perform tests of plasma levels of α-tocopherol and the confirmatory genetic test. Treatment with vitamin E decreases symptoms in both affected and presymptomatic individuals. Few patients have been described in America, and our case showed a homozygous mutation outside of high-prevalence areas. Clinical findings of this patient and a previous case would indicate that the c.205-1G>C mutation is associated with severe symptoms.