Augmentation of Water Resources Potential and Cropping Intensification Through Watershed Programs.

This paper presents the biophysical impact of various interventions made under watershed development programs, in terms of the creation of additional water resources, and resultant changes in land use and cropping patterns in the Bundelkhand region of Madhya Pradesh State, India. Both primary and secondary data gathered from randomly selected watersheds and their corresponding control villages were used in this study. Analysis revealed that emphasis was given primarily to the creation of water resources potential during implementation of the programs, which led to augmentation of surface and groundwater availability for both irrigation and non-agricultural purposes. In addition, other land based interventions for soil and moisture conservation, plantation activities, and so forth, were taken up on both arable and nonarable land, which helped to improve land slope and land use, cropping pattern, agricultural productivity, and vegetation cover.

A complete genetic linkage map and QTL analyses for bast fibre quality traits, yield and yield components in jute (Corchorus olitorius L.).

We report the first complete microsatellite genetic map of jute (Corchorus olitorius L.; 2n = 2x = 14) using an F6 recombinant inbred population. Of the 403 microsatellite markers screened, 82 were mapped on the seven linkage groups (LGs) that covered a total genetic distance of 799.9 cM, with an average marker interval of 10.7 cM. LG5 had the longest and LG7 the shortest genetic lengths, whereas LG1 had the maximum and LG7 the minimum number of markers. Segregation distortion of microsatellite loci was high (61%), with the majority of them (76%) skewed towards the female parent. Genomewide non-parametric single-marker analysis in combination with multiple quantitative trait loci (QTL)-models (MQM) mapping detected 26 definitive QTLs for bast fibre quality, yield and yield-related traits. These were unevenly distributed on six LGs, as colocalized clusters, at genomic sectors marked by 15 microsatellite loci. LG1 was the QTL-richest map sector, with the densest colocalized clusters of QTLs governing fibre yield, yield-related traits and tensile strength. Expectedly, favorable QTLs were derived from the desirable parents, except for nearly all of those of fibre fineness, which might be due to the creation of new gene combinations. Our results will be a good starting point for further genome analyses in jute.

A family with autosomal recessive generalised myotonia with Herculean appearance.

A 28-year-old male had history of stiffness in limb muscles, with hypertrophy of most muscle groups and both action and percussion myotonia. We report a very interesting rare family of brothers and sister of myotonia congenita, conforming to autosomal recessive transmission (Becker's variety) with Herculean appearance.

Multiple ring-enhancing lesions of the brain.

Multiple ring-enhancing lesions of the brain are one of the most commonly encountered abnormalities on neuroimaging. These can be caused by a variety of infectious, neoplastic, inflammatory or vascular diseases. Distinguishing non-neoplastic causes from neoplastic lesions is extremely important because a misdiagnosis can lead to unwarranted neurosurgery and exposure to toxic chemotherapy or potentially harmful brain irradiation. Diligent clinical evaluation and a battery of tests are required for making a definitive diagnosis. Newer advanced diagnostic techniques, such as diffusion-weighted magnetic resonance imaging (MRI), perfusion-weighted MRI, magnetic resonance spectroscopy, single-photon emission tomography and positron emission tomography may help in establishing the etiology. However, early brain biopsy is often needed because several of these diseases are potentially life-threatening.

Tumefactive demyelinating lesion: experience with two unusual patients.

Tumefactive demyelinating lesion, a variant of multiple sclerosis, is a solitary large demyelinating lesion, which mimics cerebral neoplasm. Distinguishing tumefactive lesions from other etiologies of intracranial space-occupying lesions is essential to avoid inadvertent surgical or toxic chemotherapeutic interventions. We report two unusual cases of tumefactive demyelinating lesion. The first patient presented with recurrent right focal tonic-clonic seizures with secondary generalization of three-month duration. Her neurological examination was normal. Another patient presented with right homonymous hemianopia. In this patient, the diagnosis was established after biopsy of the lesion, which revealed perivascular lymphocytic infiltrate and aggregates of foam cells in white matter with relatively uninvolved grey matter, suggestive of tumefactive demyelinating lesion. Administration of intravenous methylprednisolone resulted in rapid clinical improvement in both the patients and the brain lesion decreased in size. Both, epilepsy and homonymous hemianopia, are unusual manifestations of tumefactive demyelinating lesions. In our cases, cerebral tumors were initial diagnoses. Presence of an open ring or incomplete ring lesions and other magnetic resonance characteristics helped in differentiating demyelinating lesions from other neoplastic and infective diseases of the brain. Differential diagnosis of tumefactive demyelinating lesions, at times, may prove to be a challenging task for the treating physician.

Oxidative stress in hypertension: association with antihypertensive treatment.

There is growing evidence that oxidative stress contributes to the pathogenesis of hypertension. Our aim was to measure oxidative stress in hypertensive subjects, and assess the potential confounding influences of antihypertensive therapy. Serum malondialdehyde and antioxidant levels were estimated in patients at the time of presentation and also after a antihypertensive therapy for 3 months. During the period of study no antioxidant/s was given to the patients and control subjects. Mean blood pressure values were altered in the hypertensive patients following antihypertensive therapy from their respective values observed at the time of presentation. Serum malondialdehyde levels were significantly higher in the hypertensive patients in comparison to control cases. The antioxidant activity of enzymes super oxide dismutase, glutathione and non enzymatic antioxidant levels of vitamins E and C were significantly lower in patients compared to controls. After 3 months of antihypertensive treatment all the above parameters showed reversal in the respective levels of serum malondialdehyde and antioxidant activity. Antihypertensive medications lower the blood pressure and thereby results in reduced oxidative stress which indicates that oxidative stress is not the cause, but rather a consequence, of hypertension.

Entrainment of the diurnal rhythm of plasma leptin to meal timing.

To identify the physiologic factor(s) that entrain the diurnal rhythm of plasma leptin, leptin levels were measured hourly after changes in light/dark cycle, sleep/wake cycle, and meal timing. Four young male subjects were studied during each of two protocols, those being a simulated 12-h time zone shift and a 6.5-h meal shift. During the baseline day, plasma leptin demonstrated a strong diurnal rhythm with an amplitude of 21%, zenith at 2400 h, and nadir between 0900 and 1200 h. Acute sleep deprivation did not alter plasma leptin, but day/night reversal (time zone shift) caused a 12+/-2 h shift (P < 0.01) in the timing of the zenith and nadir. When meals were shifted 6.5 h without changing the light or sleep cycles, the plasma leptin rhythm was shifted by 5-7 h (P < 0.01). The phase change occurred rapidly when compared with changes in the diurnal rhythm of cortisol, suggesting that leptin levels are not acutely entrained to the circadian clock. The leptin rhythm was altered by meal timing in a manner very similar to the rhythm of de novo cholesterol synthesis. We conclude that the diurnal rhythm of plasma leptin in young males is entrained to meal timing.

Insulin-like growth factor I binding in hepatocytes from human liver, human hepatoma, and normal, regenerating, and fetal rat liver.

Insulin-like growth factor-I (IGF-I) in human hepatoma cells (HEP-G2) has, in addition to its effect on cell growth, short-term metabolic effects acting through its own receptor. We have demonstrated that normal human hepatocytes, compared with HEP-G2 cells, have virtually no IGF-I binding sites. Because the rate of growth is the major difference between the hepatoma and the normal liver, we asked if normal liver might express IGF-I binding sites under physiologic growth conditions. Indeed, whereas adult rat hepatocytes have low IGF-I binding sites similar to those in human liver, hepatocytes from regenerating liver after 3 d subtotal hepatectomy have an approximately sixfold increase (P less than 0.005) and those from fetal rat liver a approximately 12-fold increase (P less than 0.005), to levels comparable to those in the HEP-G2 cells. The specificity of 125I IGF-I binding to its receptor was demonstrated by competition studies with monoclonal antibodies directed toward the IGF-I and the insulin receptors, with unlabeled IGF-I and insulin and by affinity labeling experiments. Thus, if IGF-I has any short-term metabolic functions in the adult human liver, it is not through interaction with its own receptor. Autocrine regulation by IGF-I of liver growth appears possible since IGF-I binding sites are expressed under pathological and physiological conditions of growth. The mechanism that couples these two phenomena remains to be elucidated.

Long-term effect of insulin on glucose transport and insulin binding in cultured adipocytes from normal and obese humans with and without non-insulin-dependent diabetes.

We have tested the hypothesis that in vitro exposure of insulin-resistant adipocytes with insulin results in improved insulin action. A primary culture system of adipocytes from obese subjects with or without non-insulin-dependent diabetes mellitus (NIDDM) and nonobese control subjects has been developed. The adipocytes when cultured in serum-free medium do not lose their original characteristics in regard to insulin binding and glucose transport. The adipocytes from three groups were incubated with insulin (0, 10(-10) M, and 10(-7) M) for 24 h at 37 degrees C, receptor-bound insulin was dissociated, and basal and insulin (1 X 10(-11)-10(-7) M)-stimulated glucose transport and 125I-insulin binding were determined. The 24-h insulin exposure of adipocytes from control subjects decreased basal and insulin-stimulated glucose transport. The effects of 1 X 10(-7) M insulin were more pronounced than 1 X 10(-10) M insulin. Similarly, insulin exposure decreased insulin sensitivity and responsiveness of cultured adipocytes from obese and NIDDM patients. The insulin-induced reduction in insulin sensitivity and responsiveness for glucose transport in three groups were due to alterations at insulin binding and postbinding levels. In conclusion, insulin induces insulin resistance in control adipocytes and further worsens the insulin resistance of adipocytes from obese and NIDDM subjects. For insulin to improve the insulin resistance of adipocytes from NIDDM patients, either more prolonged in vitro insulin exposure and/or other hormonal factors might be required.

Insulin receptor kinase in human skeletal muscle from obese subjects with and without noninsulin dependent diabetes.

We have studied the structure and function of the insulin receptors in obese patients with and without noninsulin dependent diabetes mellitus (NIDDM) and in nonobese controls using partially purified receptors from muscle biopsies. Insulin binding was decreased in obesity due to reduced number of binding sites but no differences were observed in insulin binding between obese subjects with or without NIDDM. The structural characteristics of the receptors, as determined by affinity labeling methods and electrophoretic mobility of the beta-subunit, were not altered in obese or NIDDM compared to normal weight subjects. Furthermore, the ability of insulin to stimulate the autophosphorylation of the beta-subunit and the phosphoamino acid composition of the phosphorylated receptor were the same in all groups. However, insulin receptor kinase activity was decreased in obesity using Glu4:Tyr1 as exogenous phosphoacceptor without any appreciable additional defect when obesity was associated with NIDDM. Thus, our data are supportive of the hypothesis that in muscle of obese humans, insulin resistance is partially due to decreased insulin receptors and insulin receptor kinase activity. In NIDDM the defect(s) in muscle is probably distal to the insulin receptor kinase.

Studies on the mechanism of insulin resistance in the liver from humans with noninsulin-dependent diabetes. Insulin action and binding in isolated hepatocytes, insulin receptor structure, and kinase activity.

We have developed a method to isolate insulin-responsive human hepatocytes from an intraoperative liver biopsy to study insulin action and resistance in man. Hepatocytes from obese patients with noninsulin-dependent diabetes were resistant to maximal insulin concentration, and those from obese controls to submaximal insulin concentration in comparison to nonobese controls. Insulin binding per cell number was similar in all groups. However, insulin binding per surface area was decreased in the two obese groups because their hepatocytes were larger. In addition, the pool of detergent-extractable receptor was further decreased in diabetics. Insulin receptors in all groups were unaltered as determined by affinity-labeling methods. However, insulin-stimulated insulin receptor kinase activity was decreased in diabetics. Thus, in obesity, decreased surface binding could explain resistance to submaximal insulin concentrations. In diabetes, diminished insulin-stimulated protein kinase activity and decreased intracellular pool of receptors could provide an explanation for postinsulin-binding defect(s) of insulin action in human liver.

Evidence of free and bound leptin in human circulation. Studies in lean and obese subjects and during short-term fasting.

Little is known about leptin's interaction with other circulating proteins which could be important for its biological effects. Sephadex G-100 gel filtration elution profiles of 125I-leptin-serum complex demonstrated 125I-leptin eluting in significant proportion associated with macromolecules. The 125I-leptin binding to circulating macromolecules was specific, reversible, and displaceable with unlabeled leptin (ED50: 0.73 +/- 0.09 nM, mean +/- SEM, n = 3). Several putative leptin binding proteins were detected by leptin-affinity chromatography of which either 80- or 100-kD proteins could be the soluble leptin receptor as approximately 10% of the bound 125I-leptin was immunoprecipitable with leptin receptor antibodies. Significantly higher (P < 0.001) proportions of total leptin circulate in the bound form in lean (46.5 +/- 6.6%) compared with obese (21.4 +/- 3.4%) subjects. In lean subjects with 21% or less body fat, 60-98% of the total leptin was in the bound form. Short-term fasting significantly decreased basal leptin levels in three lean (P < 0.0005) and three obese (P < 0.005) subjects while refeeding restored it to basal levels. The effects of fasting on free leptin levels were more pronounced in lean subjects (basal vs. 24-h fasting: 19.6 +/- 1.9 vs. 1.3 +/- 0.4 ng/ml) compared with those in obese subjects (28.3 +/- 9.8 vs. 14.7 +/- 5.3). No significant (P > 0.05) decrease was observed in bound leptin in either group. These studies suggest that in obese individuals the majority of leptin circulates in free form, presumably bioactive protein, and thus obese subjects are resistant to free leptin. In lean subjects with relatively low adipose tissue, the majority of circulating leptin is in the bound form and thus may not be available to brain receptors for its inhibitory effects on food intake both under normal and food deprivation states.

Nocturnal rise of leptin in lean, obese, and non-insulin-dependent diabetes mellitus subjects.

We studied 24-h profiles of circulating leptin levels using a sensitive and specific RIA in lean controls and obese subjects with or without non-insulin-dependent diabetes mellitus (NIDDM) during normal routine activity. Serum leptin levels were significantly higher in obese (41.7 +/- 9.0 ng/ml; n = 11) and obese NIDDM (30.8 +/- 6.7; n = 9) subjects compared with those in lean controls (12.0 +/- 4.4, n = 6). In all the three groups, serum leptin levels were highest between midnight and early morning hours and lowest around noon to midafternoon. The nocturnal rise in leptin levels was significant when data were analyzed by ANOVA (lean: F = 3.17, P < 0.0001, n = 4; obese: F = 2.02, P < 0.005, n = 11; and obese NIDDM: F = 4.9, P < 0.0001, n = 5). The average circadian amplitude between acrophase and nadir was 75.6% in lean, 51.7%, in obese and 60.7% in obese NIDDM groups, respectively. No significant correlations (P > 0.05) were observed between circulating levels of leptin and either insulin or glucose levels in any of the 20 subjects studied for 24-h profiles. The nocturnal rise in leptin observed in the present study resembles those reported for prolactin, thyroid-stimulating hormone, and free fatty acids. We speculate that the nocturnal rise in leptin could have an effect in suppressing appetite during the night while sleeping.

Surgical challenges and outcomes of rhegmatogenous retinal detachment in albinism.

PURPOSE: To report the outcomes and surgical difficulties during rhegmatogenous retinal detachment (RRD) repair in patients with albinism. METHODS: Retrospective analysis of 10 eyes of 9 patients with albinism that underwent RRD repair was performed. Collected data included demographic details, preoperative examination details, surgical procedure, surgical difficulties, anatomical, and visual outcomes. Outcome measures were retinal reattachment and visual acuity at the last follow-up. RESULTS: Mean preoperative best-corrected visual acuity (BCVA) was logMAR (Logarithm of the Minimum Angle of Resolution) 2.15 (range 0.9-3.0) with preoperative localization of causative break in six eyes. One eye had proliferative vitreoretinopathy grade C1 preoperatively. Four eyes underwent scleral buckling (SB) and six underwent 20G pars plana vitrectomy (PPV) with silicone oil injection. Intraoperative complication as iatrogenic retinal break occurred in four eyes. For retinopexy during vitrectomy, endolaser delivery was possible in three out of six eyes, whereas three eyes had cryopexy. The mean follow-up was 12 months in SB group (range 1-12; median 12 months) and 5.33 months (range 1-12; median 3 months) in PPV group. Among vitrectomized eye, two eyes had recurrence at 3 months with oil in situ. Rest of the eyes had attached retina at last follow-up. Mean BCVA at last follow-up was logMAR -1.46 (range 0.7-2.0) with mean improvement of -0.57 logMAR. CONCLUSIONS: Identification of break, induction of posterior vitreous detachment, and endolaser delivery may be difficult during RRD repair in patients with albinism. The incidence of PVR appeared less in these eyes. Both SB and PPV were efficacious and appear to be good surgical techniques for use in this patient population.

Subunit structure, autophosphorylation, and tyrosine-specific protein kinase activity of hepatic insulin receptors in fetal, neonatal, and adult rats.

The ontogeny of the structural and functional characteristics of insulin receptors is determined by examining insulin binding, subunit structure, autophosphorylation, and tyrosine-specific protein kinase activity in partially purified solubilized liver receptors from fetal (approximately 21 days postconception), neonatal (1- and 7-day-old), and adult rats. Specific 125I-labeled insulin binding to these receptor preparations in the presence of different insulin concentrations was higher in fetal and neonatal rats compared with that in the adult rats. The electrophoretic mobilities of the alpha- and beta-subunits on sodium dodecyl sulfate-polyacrylamide gel electrophoresis autoradiography were similar at different stages of development. Insulin-stimulated autophosphorylation of insulin receptors was similar in the different groups. With fixed amounts of protein, the tyrosine-specific protein kinase activity in the presence of different insulin concentrations (1 X 10(-8) to 1 X 10(-6) M) was significantly higher in the fetal and neonatal rats than in adult rats. However, when expressed as a function of insulin-binding activity, the insulin-stimulated tyrosine-specific protein kinase activity in fetal and neonatal rats appears to be similar to that in adult rats because of decreased insulin binding in the latter group. These results demonstrate the structural and functional similarities of hepatic insulin receptors in fetal, neonatal, and adult rats. The relative differences in insulin-mediated biological functions in fetal and adult rat livers as reported previously are due to alterations in a step(s) distal to activation of insulin-receptor kinase.

Possible dissociation between insulin binding and insulin action in isolated fetal rat hepatocytes.

To directly examine the relationship between insulin receptors and insulin action in fetal tissue, we compared insulin receptor characteristics and insulin-mediated 14C-glucose incorporation into glycogen, as well as glycogen synthase activity, in freshly isolated hepatocytes from 21-day fetal (F) and adult (A) rats. Viability of hepatocytes was documented by trypan blue exclusion (greater than 90%), time-dependent 14C-leucine incorporation into protein, and dose-related incorporation of glucose into glycogen. Percent specific binding of 125I-insulin per unit protein was significantly higher in F than A liver plasma membranes (32.2 +/- 0.3 versus 18 +/- 2.4; P less than 0.01) and Scatchard plots revealed twice the number of receptors in F. Similarly, receptor number per cell surface area was threefold higher in F than in A (150 versus 50 sites/micron2). At a fixed medium glucose concentration of 11.2 mM, insulin stimulated 14C-glucose incorporation into glycogen in a dose-related manner in A with an apparent Km of 1.0 ng/ml and Vmax at 5-10 ng/ml corresponding to 30-40% of total receptor occupancy; no effect was obtained in F with insulin up to 100 ng/ml. Net glucose incorporation into glycogen (nmol/10(6) cells/h) increased progressively with increasing medium glucose concentrations ranging from 1.4 to 27.8 mM; incorporation by F was significantly greater than by A at each glucose concentration. However, whereas insulin at 100 ng/ml significantly augmented net glucose incorporation at each glucose concentration in A, no effect of insulin was apparent in F.(ABSTRACT TRUNCATED AT 250 WORDS)

Insulin-receptor kinase activity of adipose tissue from morbidly obese humans with and without NIDDM.

We have determined glucose transport, insulin binding, and insulin-receptor kinase activity in adipose tissue from morbidly obese patients with and without non-insulin-dependent diabetes mellitus (NIDDM). The insulin sensitivity and responsiveness of glucose transport in freshly isolated adipocytes were significantly reduced in NIDDM subjects compared with nondiabetics. This was due in part to decreased insulin binding in adipocytes. Reduced specific 125I-labeled insulin binding was also observed in crude detergent extracts and partially purified insulin receptors from adipose tissue. In addition, the basal and insulin-stimulated tyrosine-specific protein kinase activity per milligram of protein was significantly decreased in NIDDM patients compared with nondiabetics. The differences between maximally insulin-stimulated and basal kinase activities expressed by insulin-binding activity were also significantly reduced in NIDDM subjects. We conclude that insulin resistance in morbidly obese patients with NIDDM is due to both insulin-binding and postbinding defects. One of the postbinding defects in NIDDM appears to be impaired insulin-receptor kinase activity of fat tissue.

Mechanism of IGF-I-stimulated glucose transport in human adipocytes. Demonstration of specific IGF-I receptors not involved in stimulation of glucose transport.

We demonstrate the presence of specific insulinlike growth factor I (IGF-I) receptors in human adipocytes. Competition studies with 125I-labeled IGF-I and unlabeled IGF-I, IGF-II, and insulin showed the specificity of 125I-IGF-I binding to the IGF-I receptors in adipocytes, membranes, and partially purified detergent-solubilized extracts. The monoclonal antibody to the IGF-I receptor (alpha-IR3) inhibits 125I-IGF-I binding and immunoprecipitates the IGF-I receptor. In addition, the alpha-subunit of IGF-I receptor is approximately 10,000 Mr larger than the alpha-subunit of insulin receptor, and IGF-I stimulates phosphorylation of the beta-subunit of the IGF-I receptor. IGF-I stimulates basal glucose transport in human adipocytes, but the concentrations of IGF-I required for half-maximal and maximal stimulation of glucose transport are 800- and 1000-fold greater than that of insulin. The possibility of IGF-I stimulating glucose transport by interacting predominantly with insulin receptors is suggested by data showing that 1) IGF-I competes with insulin-binding sites, 2) there is a lack of an additive effect with IGF-I and insulin in stimulating glucose transport, 3) alpha-IR3, which specifically inhibits IGF-I binding, does not inhibit IGF-I or insulin-stimulated glucose transport, 4) insulin-receptor antibody MA-10 inhibits IGF-I and insulin-stimulated glucose transport, and 5) IGF-I stimulates insulin-receptor autophosphorylation, although its effect is markedly decreased compared with insulin. In summary, human adipocytes possess specific IGF-I receptors. However, IGF-I stimulates glucose transport predominantly by interacting with the insulin receptor.

Adipose tissue glucose transporters in NIDDM. Decreased levels of muscle/fat isoform.

We investigated the mechanism of peripheral insulin resistance in the adipose tissue of obese and non-insulin-dependent diabetes mellitus (NIDDM) patients at the level of the glucose-transport effector system. Freshly isolated adipocytes from obese nondiabetic and obese NIDDM subjects had decreased insulin sensitivity and responsiveness for glucose-transport stimulation compared with control subjects, with more pronounced changes associated with obese NIDDM patients. The relative abundance of muscle/fat glucose-transporter isoform in the three groups of subjects was determined by Western-blot analysis of detergent-soluble adipose tissue extracts with monoclonal antibody 1F8. Obesity per se had no effect on adipose tissue muscle/fat glucose-transporter isoform (3150 +/- 660 vs. 4495 +/- 410 counts/min [cpm]/mg protein). Furthermore, decreased levels of muscle/fat isoform in adipose tissue of NIDDM patients were also reflected in isolated adipocytes. Our results demonstrate that insulin resistance in isolated adipocytes of NIDDM patients could at least partly be due to a significant depletion of adipose tissue muscle/fat glucose-transporter isoform.

Oxidative stress in patients with essential hypertension.

BACKGROUND: Free oxygen radicals react with membrane lipids to form lipid hydroperoxides, a destructive process known as lipid peroxidation. Lipid hydroperoxides decompose to form a variety of products including malondialdehyde, which is used as an indicator of the oxidative damage of cells and tissues. Endogenous antioxidant enzymes such as superoxide dismutase counteract the oxidative damage from oxidative stress. There is increasing evidence that free radicals are involved in the pathogenesis of hypertension by altering endothelial function. We evaluated the oxidative stress and endogenous enzymatic antioxidant status in patients with essential hypertension before and 3 months after treatment with antihypertensives. METHODS: Fifty patients with essential hypertension attending the outpatient services of the Department of Medicine, Institute of Medical Sciences, Banaras Hindu University and 20 age- and sex-matched healthy controls were studied. The serum malondialdehyde and superoxide dismutase levels were measured in patients at the time of presentation and after 3 months of antihypertensive treatment. No antioxidants were given to the patients during the period of the study. RESULTS: The mean (SD) serum malondialdehyde level was found to be significantly higher (0.33 [0.07] mmol/L) in patients with hypertension compared with controls (0.21 [0.05] mmol/L; p < 0.001). This showed a significant decrease following antihypertensive therapy (0.23 [0.06] mmol/L; p < 0.001) compared with pre-treatment values. The serum superoxide dismutase activity was significantly lower in patients (6.93 [1.35] mg protein/ml of serum) compared with controls (20.12 [3.65] mg protein/ml serum; p < 0.001) at the time of presentation and, compared with the pre-treatment values, increased significantly after 3 months of treatment (10.66 [2.91] mg protein/ml of serum; p < 0.001). CONCLUSION: Our study shows that essential hypertension is associated with increased oxidative stress and reduced antioxidant status. Adequate control of blood pressure with antihypertensive therapy decreases oxidative stress and improves the antioxidant status in these patients.