Hydration status assessment and impinging factors among university students in the UAE.

OBJECTIVE: Insufficient water intake has been a global health concern as it is linked to numerous adverse health consequences. Risk factors for dehydration include low fluid intake, sun and heat exposure which is a key element especially in the Gulf region. The aim of this study was to identify the prevalence and the impinging factors of hypohydration among college students in UAE. SUBJECTS AND METHODS: Bioelectrical Analysis Impedance (BIA), attained using BodyStat 1,500 MDD, was used to assess participants' body water levels. Adequate hydration level was defined as body water level of 50-60% for females and 55-65% for males. Alongside this, a scale and a stadiometer were used to measure the participants' weight and height in order to calculate their BMI.  A self-administered questionnaire was also used to assess and correlate the test findings with the risk factors, signs and symptoms, and the level of knowledge awareness of the participants. RESULTS: Of the 201 university students that participated in the study, 41.3% were hypohydrated, 55.7% were well hydrated and 3% were hyper-hydrated. Among hypohydrated participants, 56.6% were females and 43.4% were males, highlighting that females were at higher risk of becoming dehydrated than males. A major factor that negatively affected hydration status was BMI; as BMI increased, water percentage and therefore hydration status decreased. We checked for numerous signs and symptoms that could indicate hypohydration levels, and the following were the top five most prevalent among our participants: dry lips (51.90%), thirst (46.90%), tiredness (46.80%), dry skin (39.70%) and headache (36.90%). According to The Urine Color Chart (Human Kinetics, Champaign, IL, USA), 3.5% were classified as dehydrated, 46% were in danger of getting hypohydration levels while 19.5% were classified as having good hydration levels. There was no significant correlation between water intake and urine colour chart (p = 0.334). Among the study participants, 64.2% acquired their knowledge from internet, 30.80% from TV and radio and 26.90% from books and courses. The behavior aspect of the participants when feeling thirsty, was that 79% of them would resort to water, while 11% resorted to soft drinks and 10% to juices. CONCLUSIONS: The prevalence of hypohydration levels was 41.3% among the study participants of young university students. The main risk factors affecting hydration levels were BMI and gender. This signifies the importance of good hydration habits which were not commonly practiced among students even though they had adequate knowledge regarding the topic. Regular check-ups held intermittently can aid in recognizing those at risk of dehydration and help in educating about the importance of such topic especially regionally.

Role of oxidative stress in angiogenesis and the therapeutic potential of antioxidants in breast cancer.

The escalation of cancer cases globally, especially breast cancer, is of concern. Angiogenesis is hallmark of cancer pathogenesis and plays an important role in cancer progression and metastasis. Pro-angiogenic agents, secreted by tumor cells, form new blood vessels, and produce reactive oxygen species (ROS). ROS promote angiogenesis via two major pathways: namely Vascular Endothelial Growth Factor (VEGF) dependent and non-VEGF dependent pathways. As a consequence of unbalanced ROS overproduction and low antioxidants levels, oxidative stress occurs and promotes angiogenesis in breast cancer tissues. Thus, the potential use of antioxidants as a preventive therapy in breast cancer. Preclinical studies depict that vitamins A and E may counter oxidative stress resulting in reduction of metastasis and viability of breast cancer. Furthermore, clinical studies demonstrate a decline in breast cancer risk in postmenopausal women upon the consumption of antioxidants. Herein, we discuss various pro-angiogenic agents that may play an important role in breast cancer angiogenesis. Moreover, the contribution of oxidative stress in inducing the angiogenic process is extensively reviewed here. Furthermore, the findings of pre-clinical and clinical studies on the use of antioxidants, namely vitamins A and E, in breast cancer are deliberated upon, along with the role of angiogenesis in cancer therapy.

Attenuation of changes in sarcoplasmic reticular gene expression in cardiac hypertrophy by propranolol and verapamil.

The effects of propranolol and verapamil on contractile dysfunction, subcellular remodeling and changes in gene expression in cardiac hypertrophy due to pressure overload were examined. Rats were subjected to banding of the abdominal aorta and then treated with either propranolol (10 mg/kg daily), verapamil (5 mg/kg daily) or vehicle for 8 weeks after the surgery. Depression of the left ventricular function in the hypertrophied heart was associated with decreases in myofibrillar and myosin Ca2+ ATPase activities as well as Ca2+-pump and Ca2+-release activities of the sarcoplasmic reticulum (SR). The level of alpha-myosin heavy chain (alpha-MHC) mRNA was decreased while that of beta-MHC mRNA was increased in the pressure-overloaded heart. The level of SR Ca2+-pump ATPase (SERCA2) mRNA and protein content for SERCA2 were decreased in the pressure overloaded heart. Treatment of the hypertrophied animals with propranolol or verapamil resulted in preservation of the left ventricular function and prevention of the subcellular alterations. Shift in the alpha- and beta-MHC mRNA levels and changes in the expression in SERCA2 mRNA level and protein content were also attenuated by these treatments. The results suggest that blockade of beta-adrenoceptors or voltage-dependent calcium channels normalizes the cardiac gene expression, prevents subcellular remodeling and thus attenuates heart dysfunction in rats with cardiac hypertrophy. Furthermore, both cardiac beta-adrenoceptors and L-type Ca2+-channels may be involved in the genesis of cardiac hypertrophy due to pressure overload.

Status of myocardial antioxidants in ischemia-reperfusion injury.

BACKGROUND: Myocardial ischemia-reperfusion represents a clinically relevant problem associated with thrombolysis, angioplasty and coronary bypass surgery. Injury of myocardium due to ischemia-reperfusion includes cardiac contractile dysfunction, arrhythmias as well as irreversible myocyte damage. These changes are considered to be the consequence of imbalance between the formation of oxidants and the availability of endogenous antioxidants in the heart. OBSERVATIONS: An increase in the formation of reactive oxygen species during ischemia-reperfusion and the adverse effects of oxyradicals on myocardium have now been well established by both direct and indirect measurements. Although several experimental studies as well as clinical trials have demonstrated the cardioprotective effects of antioxidants, some studies have failed to substantiate the results. Nonetheless, it is becoming evident that some of the endogenous antioxidants such as glutathione peroxidase, superoxide dismutase, and catalase act as a primary defense mechanism whereas the others including vitamin E may play a secondary role for attenuating the ischemia-reperfusion injury. The importance of various endogenous antioxidants in suppressing oxidative stress is evident from the depression in their activities and the inhibition of cardiac alterations which they produce during ischemia-reperfusion injury. The effects of an antioxidant thiol containing compound, N-acetylcysteine, and ischemic preconditioning were shown to be similar in preventing changes in the ischemic-reperfused hearts. CONCLUSIONS: The available evidence support the role of oxidative stress in ischemia-reperfusion injury and emphasize the importance of antioxidant mechanisms in cardioprotection.

Effects of peroxide on contractility of coronary artery rings of different sizes.

Reactive oxygen species (ROS, free radicals) produced during cardiac ischemia and reperfusion can damage the contractile functions of arteries. The sarcoplasmic reticulum (SR) Ca2+ pump in coronary artery smooth muscle is very sensitive to ROS. Here we show that contractions of de-endothelialized rings from porcine left coronary artery produced by the hormone Angiotensin II and by the SR Ca2+ pump inhibitors cyclopiazonic acid and thapsigargin correlate negatively with the tissue weight. In contrast, the contractions due to membrane depolarization by high KCl correlate positively. Peroxide also produces a small contraction which correlates negatively with the tissue weight. When artery rings are treated with peroxide and washed, their ability to contract with Angiotensin II, cyclopiazonic acid and thapsigargin decreases. Thus, the SR Ca2+ pump may play a more important role in the contractility of the smaller segments of the coronary artery than in the larger segments. These results are consistent with the hypothesis that ROS which damage the SR Ca2+ pump affect the contractile function of the distal segments more adversely than of the proximal segments.

ET(B)-mediated contraction differs between left descending coronary artery and its next branch.

Pig left descending coronary artery (main artery) and its next branch (branch arteries) differ in many properties. Here we report on the receptor types and the Ca2+ pools utilized for endothelin (ET) contraction in 3 mm long de-endothelialized rings of the main (weight 7.38 +/- 0.38 mg) and the branch (1.07 +/- 0.03 mg) arteries. KCl (60 mM) contracted the main and the branch arteries with force of 41.8 +/- 3.1 and 16.9 +/- 1.0 mN (millinewton), respectively. Force of contraction for all the other agents was normalized taking the KCl value as 100%. We determined the total ET-induced responses using ET-1 and those mediated by ET(B) using IRL1620. In Ca2+-containing solutions, ET-1 contracted the main arteries with pEC50 = 8.2 +/- 0.1 and a maximum force of 98 +/- 5%. The branch arteries also gave similar values of pEC50 (8.4 +/- 0.1) and maximum force (99 +/- 14%). IRL1620 contracted the main and the branch arteries with pEC50 = 7.9 +/- 0.1 but the maximum force was significantly higher in the branch arteries (44 +/- 3%) than in the main (15 +/- 2%). In Ca2+-free solutions, the pEC50 values for ET-1 or IRL-1620 did not change but the maximum force of contraction was diminished considerably in both main and branch arteries. Thus, the left coronary artery and its next branch differ in that the role of ET(B) receptors is greater in the latter.

Peroxide sensitivity of endothelin responses in coronary artery smooth muscle: ET(A) vs. ET(B) pathways.

Endothelins (ETs) contract de-endothelialized rings from left descending coronary artery via ET(A) or ET(B) receptors. Here we test the hypothesis that the actions of EA(A) and ET(B) receptors are similar in their sensitivities to damage by hydrogen peroxide. In Ca2+-containing Krebs' solution, 100 nM of the ET(B) agonist IRL1620 produced contractions with significantly smaller force (17.6+/-1.7 mN) than 50 nM of the ET(A) + ET(B) agonist ET-1 (73.2+/-4.6 mN) (p < 0.05). In Ca2+-free solutions, the contractions due to both agents were significantly smaller (p < 0.05). Pretreating the tissues with peroxide inhibited the contractions produced by either agent. The IC50 values for peroxide were significantly higher (p < 0.05) using ET-1 (1.0+/-0.3 mM in Ca2+, 1.4+/-0.1 mM in Ca2+-free) than using IRL 1620 (0.32+/-0.08 in Ca2+, 0.25+/-0.01 mM in Ca2+-free). Pretreating microsomes isolated from the artery smooth muscle with up to 10 mM peroxide did not significantly affect 125I-ET-1 binding to ET(A) or ET(B) receptors (p > 0.05). In comparing the peroxide induced inactivation of the various processes in this artery and based on literature, we conclude that the actions of ET(A) may also involve a peroxide resistant Ca2+-independent pathway(s).

Endothelin contraction in pig coronary artery: receptor types and Ca(2+)-mobilization.

Endothelin is one of the most potent vasoconstrictors known. It plays an important role in the regulation of vascular tone and in the development of many cardiovascular diseases. This study focuses on the receptor types and the Ca2+ mobilization responsible for endothelin-1 (ET-1) contraction in de-endothelialized pig coronary artery rings. ET-1 contracted the artery rings with an EC50 = 6.5 +/- 1 nM and a maximum contraction which was 98.6 +/- 9% of the contraction produced by 60 mM KCl. BQ123 (5 microM), an ETA antagonist, reversed 78 +/- 3% of the ET-1 contraction (50 nM). IRL1620, a selective ETB agonist, produced 23 +/- 3% of the total ET-1 contraction with an EC50 = 12.7 +/- 2 nM. More than 85% of the contraction due to 100 nM IRL 1620 was inhibited by 200 nMBQ788, an ETB antagonist. Therefore, approximately 80% of the ET-1 contraction in this artery occurred via ETA receptors, and the other 20% was mediated by ETB receptors. To assess the Ca2+ pools utilized during the ET-1 response, ET-1 contraction was also examined in medium containing an L-type Ca2+ channel blocker nitrendipine, and in Ca2+ free medium containing 0.2 mM EGTA. In Ca2+ containing medium the contraction elicited by ET-1 was 98.6 +/- 9% of the KCl contraction, however, in the presence 10 microM nitrendipine the ET-1 induced contraction was 54 +/- 7% of the KCl contraction, and in Ca(2+)-free medium it was 13 +/- 2%. Similarly, the IRL 1620 contractions in Ca2+ containing medium, in the presence of nitrendipine and in Ca(2+)-free medium were 22.4 +/- 3%, 12 +/- 3% and 11 +/- 2% of the KCl response respectively. Thus, both ETA and ETB contractions utilize extracellular Ca2+ pools via L-type Ca2+ channels and other undefined route(s), as well as intracellular Ca2+ pools. In the pig coronary artery smooth muscle, ET-1 contractions occur predominantly via ETA receptors, with ETB receptors using similar Ca2+ mobilization pathways, but the ETB receptors appear to use the intracellular Ca2+ stores to a greater extent.

SR Ca2+ pump heterogeneity in coronary artery: free radicals and IP3-sensitive and -insensitive pools.

Reactive oxygen species are known to decrease the action of agents that mobilize Ca2+ from sarcoplasmic reticulum (SR) in pig coronary artery smooth muscle. Potentially, this may be due to damage to the SR Ca2+ pump or to the myo-inositol 1,4,5-trisphosphate (IP3)-induced Ca2+ release channels. Here we report on the effects of peroxide and superoxide on the SR Ca2+ pump and the subsequent IP3-induced Ca2+ release. Smooth muscle cells cultured from pig left coronary arteries were permeabilized using saponin and then loaded with 45Ca2+ in the presence of an ATP-regenerating system and the mitochondrial Ca2+ uptake inhibitor sodium azide. IP3 caused a release of up to 65% of the loaded 45Ca2+, whereas the Ca2+ ionophore A-23187 caused a release of > 95%. The nature of the IP3-insensitive component of the Ca2+ uptake is not known. The IP3-induced Ca2+ release occurred at 0 or 37 degrees C and was complete in < 30 s. The 50% effective concentration for IP3 was 2.7 +/- 1.0 microM at pH 6.8 and 37 degrees C. At pH 7.4 the IP3-induced Ca2+ release was slightly lower than at pH 6.4-6.8. The IP3-induced release was also inhibited by Ca2+ concentration in the release medium. To investigate the effects of peroxide or superoxide, the cells were treated with these agents, washed, skinned, and then used to examine the IP3-sensitive and -insensitive Ca2+ pools under the conditions in which the IP3-sensitive pool was 60-65% of the total. Peroxide pretreatment was equipotent in inhibiting loading into the IP3-sensitive and -insensitive Ca2+ pools. In contrast, superoxide pretreatment inhibited loading into the IP3-sensitive pool but not into the IP3-insensitive pool. These data are consistent with a model in which the SR Ca2+ pumps are heterogeneous: those required to pump Ca2+ into the IP3-sensitive pool are inhibited by peroxide and superoxide, but those loading the IP3-insensitive pool are inhibited by peroxide only.

Properties of the sarcoplasmic reticulum Ca(2+)-pump in coronary artery skinned smooth muscle.

Pig coronary artery cultured smooth muscle cells were skinned using saponin. In the presence of an ATP-regenerating system and oxalate, the skinned cells showed an ATP-dependent azide insensitive Ca(2+)-uptake which increased linearly with time for > 1 h. The Ca(2+)-uptake occurred with Km values of 0.20 +/- 0.03 microM for Ca2+ and 400 +/- 34 microM for MgATP2-. Thapsigargin and cyclopiazonic acid inhibited this uptake with IC50 values of 0.13 +/- 0.02 and 0.56 +/- 0.04 microM, respectively. These properties of SR Ca(2+)-pump are similar to those reported for membrane fractions isolated from fresh smooth muscle of coronary artery and other arteries. However, optimum pH of the uptake in the skinned cells (6.2) was lower than that reported previously using isolated membranes (6.4-6.8).

Coronary artery contractility, Na(+)-pump and oxygen radicals.

Oxygen radicals accumulated during ischemia and reperfusion may affect coronary contractility by endothelium dependent and independent pathways one of which may involve Na(+)-pump. Here we report a contractility assay for Na(+)-pump in pig coronary artery and use it to examine the effects of hydrogen peroxide and superoxide. Coronary artery rings contracted in a K(+)-free Krebs solution and relaxed upon subsequent exposure to K+. The relaxation approximated a single exponential decay whose rate constant depended on [K+]2. This K(+)-induced relaxation was abolished by ouabain and was attributed to Na(+)-pump. In tissues pretreated with peroxide, the rate of relaxation of the K(+)-free contracted arteries decreased with an IC50 = 1.6 +/- 0.6 mmol/l for peroxide. Another set of tissues was pretreated with the superoxide generating system containing 0.3 mmol/l xanthine + varying concentrations of xanthine oxidase (XO) and precontracted in K(+)-free Krebs solution. The rate of the K(+)-induced relaxation decreased with IC50 = 24 +/- 8 mU/ml for XO. Thus, using the relaxation assay we conclude that exposing coronary arteries to oxygen radicals can damage Na(+)-pumps.

Free radicals uncouple the sodium pump in pig coronary artery.

Free radicals may impair vital functions of several types of tissues including coronary artery smooth muscle. Because the Na+ pump plays a key role in maintaining coronary tone, the effects of superoxide and peroxide on this protein were examined. Ouabain-sensitive Rb+ uptake by denuded coronary artery rings was used in lieu of K+ transport by this pump. It was inhibited by exposing the rings for 90 min either to peroxide [50% inhibitory concentration (IC50) = 0.56 +/- 0.18 mM] or to superoxide generated by xanthine oxidase (XO; 0.3 mM xanthine and xanthine oxidase, IC50 = 0.08 +/- 02 mU/ml). The effect of peroxide was not overcome by superoxide dismutase and that of superoxide was not prevented by catalase. K(+)-activated ouabain-sensitive hydrolysis of p-nitrophenyl phosphate in the plasma membrane-enriched fraction isolated from the coronary artery smooth muscle was monitored as the hydrolytic activity of the Na+ pump. It was inhibited by exposing the membranes only to very high concentrations of peroxide (IC50 = 9.85 +/- 3.5 mM) or XO (IC50 = 5 +/- 2 mU/ml). The exposure to 2.5 mM H2O2 or 0.5 mU/ml XO reduced the Na(+)-dependent acylphosphate levels only by 41 +/- 3 and 30 +/- 4%, respectively even though either inhibited the Rb+ uptake by > 80%. Thus superoxide and peroxide uncoupled the hydrolytic activity of the Na+ pump from Rb+ uptake. We speculate that such an uncoupling in ischemia and reperfusion would result in dual damage: ion imbalance and continuous hydrolysis of ATP in the cells that are already starved.

Enalapril suppresses normal accumulation of elastin and collagen in cardiovascular tissues of growing rats.

We have investigated the effect of enalapril, an angiotensin converting-enzyme (ACE) inhibitor, on the accumulation of ventricular and vascular collagen and elastin in young, growing rats. Beginning at either 4 or 10 wk of age, male Wistar rats were treated with enalapril for 2 or 5 wk. Enalapril treatment had no significant effect on body weight and small, generally non-significant effects on systolic and diastolic blood pressures. In contrast, young enalapril-treated animals showed a marked decrease in accumulation of total elastin and collagen in both large (aorta, renal, and carotid) and smaller (superior and large mesenteric) arteries, as well as a large reduction in total collagen in both left and right ventricles. This effect also was present but less pronounced in rats treated with enalapril beginning at 10 wk of age. These data indicate that inhibition of ACE activity during a period of rapid growth significantly reduces accumulation of vascular and ventricular connective tissue and suggests that angiotensin II may be important in normal cardiovascular development and growth.

Effects of antihypertensive drug classes on regression of connective tissue components of hypertension.

Hypertension leads to structural and functional adaptations which, although initially protective for the cardiovascular system, ultimately work to sustain and reinforce the hypertensive state. Although blood pressure (BP) may be effectively lowered by a variety of treatments, it is becoming clear that these structural adaptation, and the risks and consequences of hypertension, may persist long after BP has been restored to normal levels. Cardiovascular tissues appear to be highly sensitive to increased BP, responding quickly with large and proportional increases in collagen and elastin. The sensitivity of this response to increased pressure, together with the slow turnover of these connective tissue proteins, suggests a mechanism by which transient or intermittent episodes of hypertension may lead to cumulative and persistent structural changes in cardiovascular tissues. With some exceptions, studies directly investigating the reversibility of these connective tissue changes have generally confirmed that increased cardiovascular collagen and elastin persist for long periods of time after BP lowering, independent of the treatment method used to achieve that lowering. Because maintenance of elevated levels of collagen and elastin is principally caused by the slow turnover of the proteins rather than by their continued production, rapid and effective reversal of cardiovascular connective tissue changes may require the development of pharmacological agents that promote or accelerate the turnover of these proteins.