A soybean based-diet prevents Cadmium access to rat cerebellum, maintaining trace elements homeostasis and avoiding morphological alterations.

Cadmium (Cd) is one of the most dangerous heavy metals that exists. A prolonged exposure to Cd causes toxic effects in a variety of tissues, including Central Nervous System (CNS), where it can penetrate the Blood Brain Barrier (BBB). Cd exposure has been linked to neurotoxicity and neurodegenerative diseases. Soy isoflavones have a strong antioxidant capacity, and they have been shown to have positive effects on cognitive function in females. However, the mechanisms underlying Cd neurotoxicity remain completely unresolved. The purpose of this study was to characterize the potential protective effect of a soy-based diet vs. a casein-based diet against Cd toxicity in rat cerebellum. Female Wistar rats were fed with casein (Cas) or soybean (So) as protein sources for 60 days. Simultaneously, half of the animals were administered either 15 ppm of Cadmium (CasCd and SoCd groups) in water or regular tap water as control (Cas and So groups). We analyzed Cd exposure effects on trace elements, oxidative stress, cell death markers, GFAP expression and the histoarchitecture of rat cerebellum. We found that Cd tissue content only augmented in the Cas intoxicated group. Zn, Cu, Mn and Se levels showed modifications among the different diets. Expression of Nrf-2 and the activities of CAT and GPx decreased in Cas and So intoxicated groups,while 3-NT expression increased only in the CasCd group. Morphometry analyses revealed alterations in the purkinje and granular cells morphology, decreased number of granular cells and reduced thickness of the granular layer in Cd-intoxicated rats, whereas no alterations were observed in animals under a So diet. In addition, mRNA expression of apoptotic markers BAX/Bcl-2 ratio and p53 expression increased only in the CasCd group, a finding confirmed by positive TUNEL staining in the cerebellum granule cell layer in the same group. Also, Cd intoxication elicited overexpression of GFAP by astrocytes, which was prevented by soy. White matter alterations were only subtle and characterized by intramyelinic edema in the CasCd group. Overall, these results unmask an irreversible toxic effect of a subchronic Cd intoxication on the cerebellum, and identify a protective role by a soy-based diet with potential as a therapeutic strategy for those individuals exposed to this dangerous environmental contaminant.

Perinatal Glyphosate-Based Herbicide Exposure in Rats Alters Brain Antioxidant Status, Glutamate and Acetylcholine Metabolism and Affects Recognition Memory.

Glyphosate-based herbicides (Gly-BHs) lead the world pesticide market. Although are frequently promoted as safe and of low toxicity, several investigations question its innocuousness. Previously, we described that oral exposure of rats to a Gly-BH during pregnancy and lactation decreased locomotor activity and anxiety in the offspring. The aim of the present study was to evaluate the mechanisms of neurotoxicity of this herbicide. Pregnant Wistar rats were supplied orally with 0.2 and 0.4% of Gly-BH (corresponding to 0.65 and 1.30 g/l of pure Gly, respectively) from gestational day (GD) 0, until weaning (postnatal day, PND, 21). Oxidative stress markers were determined in whole brain homogenates of PND90 offspring. The activity of acetylcholinesterase (AChE), transaminases, and alkaline phosphatase (AP) were assessed in prefrontal cortex (PFC), striatum, and hippocampus. Recognition memory was evaluated by the novel object recognition test. Brain antioxidant status was altered in Gly-BH-exposed rats. Moreover, AChE and transaminases activities were decreased and AP activity was increased in PFC, striatum and hippocampus by Gly-BH treatment. In addition, the recognition memory after 24 h was impaired in adult offspring perinatally exposed to Gly-BH. The present study reveals that exposure to a Gly-BH during early stages of rat development affects brain oxidative stress markers as well as the activity of enzymes involved in the glutamatergic and cholinergic systems. These alterations could contribute to the neurobehavioral variations reported previously by us, and to the impairment in recognition memory described in the present work.

Daily rhythms of catalase and glutathione peroxidase expression and activity are endogenously driven in the hippocampus and are modified by a vitamin A-free diet.

OBJECTIVES: Alterations in enzymatic antioxidant defense systems lead to a deficit of cognitive functions and altered hippocampal synaptic plasticity. The objectives of this study were to investigate endogenous rhythms of catalase (CAT) and glutathione peroxidase (GPx) expression and activity, as well as CREB1 mRNA, in the rat hippocampus, and to evaluate to which extent the vitamin A deficiency could affect those temporal patterns. METHODS: Rats from control and vitamin A-deficient (VAD) groups received a diet containing 4000 IU of vitamin A/kg diet, or the same diet devoid of vitamin A, respectively, during 3 months. Rats were maintained under 12-hour-dark conditions, during 10 days before the sacrifice. Circadian rhythms of CAT, GPx, RXRγ, and CREB1 mRNA levels were determined by reverse transcriptrase polymerase chain reaction in hippocampus samples isolated every 4 hours during a 24-hour period. CAT and GPx enzymatic activities were also determined by kinetic assays. Regulatory regions of clock and antioxidant enzymes genes were scanned for E-box, RXRE, and CRE sites. RESULTS: E-box, RXRE, and CRE sites were found on regulatory regions of GPx and CAT genes, which display a circadian expression in the rat hippocampus. VAD phase shifted CAT, GPx, and RXRγ endogenous rhythms without affecting circadian expression of CREB1. DISCUSSION: CAT and GPx expression and enzymatic activity are circadian in the rat hippocampus. The VAD affected the temporal patterns antioxidant genes expression, probably by altering circadian rhythms of its RXR receptors and clock factors; thus, it would impair the temporal orchestration of hippocampal daily cognitive performance.

Daily oscillation of glutathione redox cycle is dampened in the nutritional vitamin A deficiency.

Examples of hormonal phase-shifting of circadian gene expression began to emerge a few years ago. Vitamin A fulfills a hormonal function by binding of retinoic acid to its nuclear receptors, RARs and RXRs. We found retinoid- as well as clock-responsive sites on regulatory regions of Glutathione reductase (GR) and Glutathione peroxidase (GPx) genes. Interestingly, we observed retinoid receptors, as well as GSH, GR and GPx, display daily oscillating patterns in the rat liver. We also found that feeding animals with a vitamin A-free diet, dampened daily rhythms of RARα and RXRß mRNA, GR expression and activity, GSH, BMAL1 protein levels and locomotor activity. Differently, day-night oscillations of RXRα, GPx mRNA levels and activity and PER1 protein levels, were phase-shifted in the liver of vitamin A-deficient rats. These observations would emphasize the importance of micronutrient vitamin A in the modulation of biological rhythms of GSH and cellular redox state in liver.

Myocardial oxidative stress following sub-chronic and chronic oral cadmium exposure in rats.

We investigated the effect of oral cadmium intoxication on the antioxidant/prooxidant status in serum and heart. Wistar rats, separated into four groups, that received: (1) tap water for 60 days (control); (2), (3) and (4) Cd(2+) (15 ppm)-containing water, during 15, 30 and 60 days, respectively. Lipoperoxidation increased in serum and heart of group 4. Circulating paraoxonase-1 activity was higher in groups 2 and 3. Protein carbonyl-groups increased while total and reduced glutathione levels decreased in the heart after 15 days of cadmium intoxication. Cardiac catalase activity was higher in groups 3 and 4 but glutathione peroxidase activity diminished in the heart of all poisoned groups. Superoxide dismutase transcript levels as well as Nrf2 expression also increased in the heart of groups 2 and 3, while gp91phox and p47phox mRNA levels rose only in group 3. We suggest cadmium intoxication modifies antioxidant/prooxidant ratio in serum and heart in a time-of-exposure-dependent way.

Antioxidant properties of Amaranthus hypochondriacus seeds and their effect on the liver of alcohol-treated rats.

Amaranth constitutes a valuable pseudocereal, due to its nutritional quality and its nutraceutical properties, which contribute to improve human health. This work evaluated the effect of a diet based on Amaranthus hypochondriacus (Ah) seed on oxidative stress and antioxidant status in the liver of rats sub-chronically exposed to ethanol. The seed extract was investigated for antioxidant capacity in vitro, showing an adequate content of total phenols and antioxidant activity elevated. For in vivo assays, four groups of six rats each were fed with an AIN-93 M diet for 28 days. In groups III and IV casein was replaced by Ah as the protein source; groups II and IV were received ethanol in the drinking water (20% v/v). When comparing groups IV and II, the following was observed: significant decrease in the activity of aspartate aminotransferase and content of malondialdehyde (p<0.001) in serum; decrease of malondialdehyde and increase in the activity and gene expression of Cu,Zn-superoxide dismutase, also, decrease in the NADPH oxidase transcript levels (p<0.05) in liver. Our data suggest that Ah is a good source of total phenols and exerts a protective effect in serum and in liver of rats intoxicated with ethanol.

Cadmium exposure modifies lactotrophs activity associated to genomic and morphological changes in rat pituitary anterior lobe.

Cadmium (Cd) is widely used in industrial applications and is an important contaminant of agricultural products. As an endocrine disruptor, Cd modifies the hormone release of pituitary anterior lobe (PAL). This work was undertaken to evaluate a possible association between phospholipase D (PLD) and prolactin mRNA expressions and the activity of lactotrophs and folliculostellate cells (FSC) in PAL of Cd exposed adult male Wistar rats (Cd, 0.133 mM per liter for 2 months). The PALs were submitted to immunohistochemical and morphometric analysis to determine the percentage of lactotrophs (PRL-ir) and FSC (S-100-ir). Cultured PAL cells were stained with Hoechst 33258 to determine the presence of alterations in nuclear morphology consistent with apoptosis. The expressions of PLD and prolactin mRNA were assessed by RT-PCR. Cd treated rats showed a decrease of PLD mRNA levels that can be associated to both high number of apoptotic cells and increase of S-100 protein expression in FSC. Cd decreased prolactin mRNA expression, number of lactotrophs and percentage of PRL-ir suggesting a low availability of prolactin to be secreted from PAL. Cd modifies the lactotrophs activity of pituitary gland through biochemical, genomic and morphological changes and contributes directly or indirectly to the levels of serum prolactin.

Serum oxidative stress parameters of women with hypothyroidism.

In order to study the effects of hypothyroidism on parameters of oxidative stress in woman, we determined the values of thiobarbituric acid reactive substances (TBARS), Nitric Oxide (NO) and Paraoxonase (PON-1) using phenylacetate as substrates in serum. Women in fertile age were separated into three groups: a- euthyroidism (ET) control group, b- overt hypothyroidism (OHT) and c- subclinical hypothyroidism (SHT). TBARS concentration and the PON-1 activity as aryl esterase activity did not show differences between OHT, SHT and ET woman. The concentration of NO increased in OHT compared to ET. The SHT and ET NO values were not significantly different, but the NO level was higher in the serum of OHT compared to SHT. The OHT selectively increased the NO levels but did not modify the parameters of oxidative stress in the serum of fertile-age women.

Effect of nutritional vitamin A deficiency on lipid metabolism in the rat heart: Its relation to PPAR gene expression.

OBJECTIVE: We studied the effect of dietary vitamin A deprivation on lipid composition and mRNA expression of regulatory enzymes involved in rat heart energetic lipid metabolism and its relation to the expression of peroxisome proliferator-activated receptor (PPAR) and retinoid X receptor (RXR) genes. METHODS: Male Wistar 21-d-old rats were fed for 3 mo with a vitamin A-free diet (vitamin A-deficient group) and the same diet plus 8 mg of retinol palmitate per kilogram of diet (control group). One group of deficient animals received the control diet 15 d before sacrifice (vitamin A-refed group). Heart ventricular and mitochondrial lipid contents were determined. Lipid synthesis was measured using radioactive precursors and acetyl-coenzyme A carboxylase and mitochondrial carnitine palmitoyltransferase-I (CPT-I) activities using radioactive substrates. Fatty acid composition of mitochondrial phospholipids was analyzed by gas-liquid chromatography. Heart expression of acetyl-coenzyme A carboxylase, CPT-I, PPAR-alpha, PPAR-beta, RXR-alpha, and RXR-beta was assessed by reverse transcriptase polymerase chain reaction, and CPT-I expression was also measured by real-time polymerase chain reaction. RESULTS: Vitamin A deficiency induced changes in heart ventricular lipid content and synthesis. Mitochondrial cardiolipin decreased and the proportion of phospholipids/saturated fatty acids increased. Heart activity and mRNA levels of CPT-I and expression of PPAR-alpha and PPAR-beta genes were enhanced, whereas acetyl-coenzyme A carboxylase activity diminished. Furthermore, vitamin A deficiency decreased heart mRNA levels of RXRs. Vitamin A refeeding reverted most of the observed changes. CONCLUSION: Lipid metabolism is significantly modified in hearts of vitamin A-deficient rats. Alteration of mitochondrial energetic processes by modifying the activity and gene expressions of the regulatory enzymes is associated with a high PPAR expression induced by vitamin A deprivation.

Vitamin A deficiency injures liver parenchyma and alters the expression of hepatic extracellular matrix.

Vitamin A is an essential lipid-soluble nutrient that is crucial for morphogenesis and adult tissue maintenance. The retinoid homeostasis in the liver depends on a regular supply of vitamin A from an adequate dietary intake to preserve the normal organ structure and functions. This study focuses on the effect of vitamin A deficiency on the morphology and extracellular proteins expression of the liver in adult Wistar rats. Animals were fed with a normal (control group) or deficient vitamin A diet for 3 months. At the end of the experimental period, histological examination of the livers under light and electron microscopy revealed that vitamin A deficiency produced a loss of hepatocyte cord disposition with an irregular parenchymal organization. Abundant fat droplets were present in the cytoplasm of the hepatocytes. Elongated myofibroblastic-like cells with an irregular cytoplasmic process and without lipid droplets could be seen at the perisinusoidal space, where an elevated intensity of alpha smooth muscle actin (alpha-SMA) was observed. These results suggest that an activation of hepatic stellate cells (HSCs) occurred. Moreover, immunochemical methods revealed that vitamin A deficiency led to an increased expression of hepatic fibronectin, laminin and collagen type IV. We propose that vitamin A deprivation caused liver injury and that HSCs underwent a process of activation in which they produced alpha-SMA and synthesized extracellular components. These changes may be a factor predisposing to liver fibrosis. In consequence, vitamin A deprivation could affect human and animal health.

Effects of chronic exposure to cadmium on prostate lipids and morphology.

Cadmium is an environmental toxic metal implicated in human prostate carcinogenesis. The mechanism of its toxicity is not fully understood. Previously, we showed that cadmium exposure induces oxidative stress, especially lipid peroxidation. This study evaluates the effect of chronic exposure to 0.886 mM of cadmium (Cd) per liter in the drinking water on prostate lipid content and metabolism in Wistar rats. We determined the lipid profile and measured the expression of lipogenic enzymes: FAS, GPAT, LPL, DGAT-1, DGAT-2, ACO, CPT-1 and CT, and of certain factors involved in lipid regulation and fatty acid transporters: FAT/CD36, E-FABP, SREBP-2, PPAR-gamma and PPAR-alpha by RT-PCR. Ultrastructure was analyzed by electron microscopy and, as prostate is an androgen controlled gland, AR expression was measured by RT-PCR and Western blot. Cd altered the prostatic lipid profile. Triglycerides (TG) and esterified cholesterol (EC) decreased, free cholesterol (FC) and phospholipids (PL) increased and total cholesterol (TC) did not change. FAS, MDH and IDH activities did not vary but G6PDH decreased significantly in Cd group. Regarding TG synthesis, DGAT-1 decreased while GPAT increased and FAS, LPL and DGAT-2 remained unchanged. Regarding beta oxidation, CPT-1 increased while ACO expression decreased in Cd group. In the PL pathway, CT expression was increased. All these results would justify the decrease of TG in Cd group when compared to control. In the cholesterol metabolic pathway, HMGCoAR and SREBP-2 increased. PPAR-alpha increased but PPAR-gamma did not change. Regarding fatty acid transporters, FAT/CD36 decreased, while E-FABP increased. AR mRNA and protein expression decreased. Ultrastructural analysis showed a decrease in lipid droplets and signs of cellular damage in the Cd group. Cadmium exposure induces important changes in prostatic lipid profile and metabolism, confirmed by the morphology analyses, which also showed signs of cellular damage. These results could be important to further understanding the complex mechanism of cadmium toxicity in prostate and in the development of better treatments for people and animals exposed to the heavy metal.

Zn-limited diet modifies the expression of the rate-regulatory enzymes involved in phosphatidylcholine and cholesterol synthesis.

Suboptimal intake of Zn is one of the most common nutritional worldwide problems. Previously, we showed that Zn deficiency produces alterations in lung lipid metabolism in rats. We studied the effect of a Zn-limited (ZL) diet on the expression of the enzymes involved in phosphatidylcholine and cholesterol synthesis. After 2 months of treatment with a ZL diet we found important variations in the lipid content of Wistar male rats: triacylglycerol (TG) decreased 60% (P<0.001) while esterified cholesterol (EC), free cholesterol and phospholipids (PL) increased 66%, 24 % and 25% respectively. We also observed a decrease of 40 % in the amount of (3)H incorporated into TG and an increase of 47% and 28% in the (3)H incorporated to PL and EC respectively. Fatty acid synthase and glucose-6-phosphate dehydrogenase activity was increased (P<0.01 and P<0.05 respectively). Glycerol-3-phosphate acyltransferase, lipoprotein lipase, diacyl glycerol acyl transferase and 3-hydroxy-3-methylglutaryl CoA reductase expression decreased (P<0.01 in all cases), while acetyl CoA carboxylase and cholinephosphate cytidylyltransferase increased (P<0.01 and P<0.005 respectively). These results suggest that ZL alters the expression of enzymes involved in phosphatidylcholine and cholesterol synthesis, which could lead to increased PL and cholesterol and decreased TG. This study suggests that major changes in the lipid composition of lung are induced by a ZL condition. Therefore, Zn deficiency must be taken into account in order to design therapies and public health interventions, such as Zn supplementation for high-risk subjects or certain diseases, such as asthma.

Vitamin A deficiency induces prooxidant environment and inflammation in rat aorta.

We evaluated whether nutritional vitamin A deficiency generates oxidative stress and inflammation in aorta. Wistar male rats (21 days old) were given free access to a control (8 mg retinol as retinyl palmitate/kg) or a vitamin A- deficient diet for three months. One group of deficient animals was fed with the control diet fifteen days before sacrifice. Thiobarbituric acid-reactive substances (TBARS) and nitrite concentration where both analyzed in serum and aorta. Aorta Copper-Zinc Superoxide dismutase (CuZnSOD), Glutathion peroxidase (GPx) and Catalase (CAT) activities were measured. In addition, binding activity of the nuclear factor- kB (NF-kB), inducible and endothelial Nitric Oxide synthase (iNOS and eNOS, respectively) and Ciclooxygenase-2 (COX-2) expressions were determinated in aorta. Rats fed the vitamin A- deficient diet were characterized by sub-clinical plasma retinol concentration and showed increased serum and aorta concentrations of TBARS compared to controls. Lower than control activities of CuZnSOD, GPx, and CAT were observed in aorta of the vitamin A- deficient group. The binding activity of NF- kB was higher in vitamin A- deficient animals than controls. In addition, NO production evaluated as nitrite concentration increased in aorta and serum, associated with a higher expression of iNOS, eNOS and COX-2 in aorta of vitamin A-deficient rats. The incorporation of vitamin A into the diet of vitamin A-deficient rats reverted the changes observed in TBARS level, CuZnSOD and GPx activities, nitrite concentration and also, iNOS, eNOS and COX-2 expression. Prooxidant environment and inflammation are induced by vitamin A deficiency in rat aorta.

Alterations in the lipid content of pituitary gland and serum prolactin and growth hormone in cadmium treated rats.

The present study was undertaken to assess whether chronic exposition to cadmium (Cd, 0.133 mM per liter for 2 months) through drinking water may affect the lipid contents in the pituitary anterior lobe (PAL) of adult male Wistar rats. As compared to metal non-exposed controls, PALs exposed to cadmium showed an increase in total phospholipid contents, which was associated to an increase of the incorporation of [1-14C]-methyl choline into phosphatidylcholine and of [U-14C]-glucose into total phospholipids. The incorporation of [1-14C]-methyl choline into sphingomyelin was not changed. Incorporation of [1-14C]-acetate into total fatty acids also increased but incorporation of [1-14C]-acetate into cholesterol did not change. The activity of phospholipase D decreased both in PALs from Cd exposed rats and in PAL dispersed cells treated with Cd in the culture medium from Cd non-exposed rats. In PALS from Cd exposed rats, a decrease of serum prolactin and growth hormone concentrations was determined. The results shown that cadmium modifies the lipid contents of pituitary gland and directly or indirectly the levels of prolactin and growth hormone in serum.

Effect of the herbicide glyphosate on liver lipoperoxidation in pregnant rats and their fetuses.

Glyphosate is a post-emergence herbicide that acts on the synthesis of amino acids and other endogenous metabolites in plants. It is commonly used in agriculture, forestry, and nurseries for the control or destruction of herbaceous plants. Metabolic processes during development and pregnancy could be sensitive to changes induced by glyphosate such as lipid peroxidation. The present study has investigated the effects that 1% glyphosate oral exposure has on lipoperoxidation and antioxidant enzyme systems in the maternal serum and liver of pregnant rats and their term fetuses at 21 days of gestation. The results suggest that excessive lipid peroxidation induced with glyphosate ingestion leads to an overload of maternal and fetal antioxidant defense systems.

Morphological changes and oxidative stress in rat prostate exposed to a non-carcinogenic dose of cadmium.

Cadmium chloride is an environmental toxicant implicated in human prostate carcinogenesis. The mechanism of its toxicity is far from fully understood. This study evaluates the effect of exposure to an oral non-carcinogenic dose of cadmium (15 ppm in drinking water for three months) on different parameters of the ventral prostatic lobe of normal and exposed rats. We analyzed the histology by optic light microscopy, activities of antioxidant enzymes (CAT, SOD, GPx and G-6-PDH), expression of iNOS and COX-2 by Western blot, expression of MT-I, MT-II, IGF-I, IGF-BP5 and rtert by RT-PCR. Histological changes were found: the height of the cells decreased, acinar lumen were enlarged and they lost the typical invaginations. Lipoperoxidation was increased in the Cd group and the antioxidant enzymes changed their activities: SOD increased, CAT and G-6-PDH decreased and GPx did not show variations. iNOS and COX-2 did not change their expressions. MT-I and IGF-BP5 mRNA increased while MT-II, IGF-I and rtert did not show variations. Cd exposure induces important morphological changes in the prostate, which could be a consequence of lipoperoxidation and oxidative stress, which are not related to iNOS and COX-2. The histology suggests an involution state of the gland, confirmed by the expression of IGF-I, IGF-BP5 and rtert.

Induction of redox changes, inducible nitric oxide synthase and cyclooxygenase-2 by chronic cadmium exposure in mouse peritoneal macrophages.

Redox changes and the secretion of inflammatory mediators were investigated in resident peritoneal macrophages of mice chronically exposed to cadmium (Cd, 15 ppm for 2 months) through drinking water. Our results showed that in vivo Cd exposure altered the redox balance in mouse peritoneal macrophages, leading to excessive production of reactive oxygen species (ROS) that overwhelmed the antioxidant defenses. It also led to increased lipid peroxidation and arachidonic acid (AA) release, higher nitric oxide and prostaglandin E(2) (PGE(2)) production, and induction of inducible nitric oxide synthase and cyclooxygenase-2 compared with control macrophages. Oxidative stress and inflammation could be important processes operating in the modulation of mouse macrophage physiology induced by chronic Cd exposure.

Incidencia de la ß-talasemia en San Luis, Argentina: índices hematimétricos en la diferenciación entre ß-talasemia y anemia ferropénica / The frecuency of ß-thalassemia in San Luis, Argentina: hematimetric indexs in the differentiation between ß-thelassemia and ferropenic anemia

A fin de determinar la incidencia de la ß-talasemia en la provincia de San Luis, se analizaron 4400 muestras de pacientes que asistieron a hospitales públicos de toda la provincia. Se detectaron 390 anemias microcíticas (8.86 por ciento) de las cuales 7 resultaron ß-talasemia (0.16 por ciento del total) las que presentaron Hb A2 mayor de 3.5 por ciento. Para determinar las diferencias entre pacientes ferropénicos y ß-talasémicos se analizaron los datos de índices hematimétricos, hierro sérico, ferritina, transferrina, protoporfirina libre eritrocitaria, reticulocitos y HbA2. En pacientes talasémicos se observó que no hubo diferencias significativas en el valor de los índices hematimétricos respecto de los controles y ferropénicos, excepto que incrementó significativamente el contenido de reticulocitos y de HbA2. En pacientes ferropénicos se observó un incremento significativo de los valores de RDW y de protoporfirinas libres eritrocitarias respecto de los talasémicos y los controles. La incidencia de la ß-talasemia en la provincia de San Luis es de 1,6 por cada 1000 habitantes, la cual resulta inferior a la observada en otras provincias, probablemente por las corrientes migratorias que habitaron la región (AU)

Incidencia de la ß-talasemia en San Luis, Argentina: índices hematimétricos en la diferenciación entre ß-talasemia y anemia ferropénica / The frecuency of ß-thalassemia in San Luis, Argentina: hematimetric indexs in the differentiation between ß-thelassemia and ferropenic anemia

A fin de determinar la incidencia de la ß-talasemia en la provincia de San Luis, se analizaron 4400 muestras de pacientes que asistieron a hospitales públicos de toda la provincia. Se detectaron 390 anemias microcíticas (8.86 por ciento) de las cuales 7 resultaron ß-talasemia (0.16 por ciento del total) las que presentaron Hb A2 mayor de 3.5 por ciento. Para determinar las diferencias entre pacientes ferropénicos y ß-talasémicos se analizaron los datos de índices hematimétricos, hierro sérico, ferritina, transferrina, protoporfirina libre eritrocitaria, reticulocitos y HbA2. En pacientes talasémicos se observó que no hubo diferencias significativas en el valor de los índices hematimétricos respecto de los controles y ferropénicos, excepto que incrementó significativamente el contenido de reticulocitos y de HbA2. En pacientes ferropénicos se observó un incremento significativo de los valores de RDW y de protoporfirinas libres eritrocitarias respecto de los talasémicos y los controles. La incidencia de la ß-talasemia en la provincia de San Luis es de 1,6 por cada 1000 habitantes, la cual resulta inferior a la observada en otras provincias, probablemente por las corrientes migratorias que habitaron la región