Differential renal proteomics analysis in a novel rat model of iodinated contrast-induced acute kidney injury.

Contrast-induced acute kidney injury (CI-AKI), which occurs after the use of iodinated contrast media, has become the third leading cause of hospital-acquired acute kidney injury (AKI). It is associated with prolonged hospitalization and increased risks of end-stage renal disease and mortality. The pathogenesis of CI-AKI is unclear and effective treatments are lacking. By comparing different post-nephrectomy times and dehydration times, we constructed a new, short-course CI-AKI model using dehydration for 24 h two weeks after unilateral nephrectomy. We found that the low-osmolality contrast media iohexol caused more severe renal function decline, renal morphological damage, and mitochondrial ultrastructural alterations compared to the iso-osmolality contrast media iodixanol. The shotgun proteomics based on Tandem Mass Tag (TMT) was used to conduct proteomics research on renal tissue in the new CI-AKI model, and 604 distinct proteins were identified, mainly involving complement and coagulation cascade, COVID-19, PPAR signalling pathway, mineral absorption, cholesterol metabolism, ferroptosis, staphylococcus aureus infection, systemic lupus erythematosus, folate biosynthesis, and proximal tubule bicarbonate reclamation. Then, using parallel reaction monitoring (PRM), we validate 16 candidate proteins, of which five were novel candidates (Serpina1, Apoa1, F2, Plg, Hrg) previously unrelated to AKI and associated with an acute response as well as fibrinolysis. The pathway analysis and 16 candidate proteins may help to discover new mechanisms in the pathogenesis of CI-AKI, allowing for early diagnosis and outcome prediction.

Heat Stress Nephropathy: What Have We Learned?

The unbearable heat waves that we are experiencing these days around the world are the result of increasing global warming, leading to heat stress and a constant health issue for the existing population. The thermoregulatory dysfunction of the human body due to climatological changes might result in fluid and electrolyte imbalance and transforms the human body from a normal physiological condition to a distorted pathological state. Subsequently, at one point in time, the human body may fail to handle its normal thermoregulatory function in the form of sudden unconsciousness and health defects. There might be associated dehydration that imposes renal damage, even to the extent to cause acute kidney injury (AKI), followed by chronic kidney disease (CKD). Thus, we cannot deny CKD as a major cause of death, mainly in patients having long-standing medical issues such as cardiac dysfunction, hypertension, diabetes, and obesity, heat stress nephropathy (HSN) might therefore become a major health problem. There is always a hopeful way in our hands, fortunately, which is of course prevention, that comes through government policies and human awareness. The present review brings out light on the alarming resultant facts of heat stress, dehydration, its pathology, molecular derangements, and recommendations for the prevention of heat stress nephropathy.

Objective evaluation of chest findings in infants by postmortem computed tomography.

PURPOSE: The purpose of this study was to review the findings of computed tomography (CT) performed early postmortem on infants and to clarify the postmortem CT lung findings that occur in the absence of abnormal histopathological findings. MATERIALS AND METHODS: From July 2016 to March 2022, 72 infants were autopsied with postmortem CT (41 boys 31 girls, aged 0-36 (mean 8.2) months). Autopsy and postmortem CT lung findings were compared with the causes of death identified by the autopsies, namely sudden infant death syndrome (n = 37), acute circulatory system disease (18), drowning (7), asphyxia (5), and dehydration/undernutrition (5). RESULTS: The %aerated lung volume (-700 HU or less) ranged from 0 % to 33 % (mean 1.5 %, median 0 %), being <1 % in 61 cases (84.7 %) and >3 % in 3/5 (60 %) of the dehydration/undernutrition group. The dehydration/undernutrition group showed significant preservation of lung field air content compared with the other causes of death groups (p < 0.05). Receiver characteristic curve analysis showed a cut off value of 0.8 % and area under the curve of 0.88806. The drowning group had significantly greater pleural cavity fluid retention than the other causes of death groups (p < 0.05). No correlation was found between postmortem interval and pleural cavity fluid retention. However, resuscitation time and pleural cavity fluid retention were correlated. CONCLUSION: Evaluation of CT values on postmortem lung fields of infants usually reveals a marked decrease in air content. When air content exceeds 0.8% on infant postmortem CT, dehydration/undernutrition should be considered in the differential diagnosis.

Magnetic resonance imaging of inflammatory pseudotumor of the liver: a 2021 systematic literature update and series presentation.

PURPOSE: Inflammatory pseudotumors of the liver (IPTL) are not exceptional benign lesions with various etiologies, histology, and imaging appearances. The incomplete knowledge of this pathology and the wide polymorphism sometimes resembling malignancy often induce long and expensive diagnostic flow, biopsy and occasionally unnecessary surgery. We propose a systematic revision of MRI literature data (2000-2021) with some narrative inserts and 10 new complete MRI cases, with the aim of organizing the data about IPTL and identifying some typical features able to improve its diagnosis from imaging. METHODS: We performed a systematic revision of literature from 2000 to 2021 to obtain MRI features, epidemiological, and clinical data of IPTL. The basic online search algorithm on the PubMed database was "(pseudotumor) AND (liver) AND (imaging)." Quality assessment was performed using both scales by Moola for case report studies and by Munn for cross-sectional studies reporting prevalence data. A case-based retrospective study by collecting patients diagnosed with IPTL from three different university hospitals from 2015 to 2021 was done as well. Only cases with MR examinations complete with T1/T2/contrast-enhanced T1/Diffusion-Weighted (W) images and pathology-proven IPTL were selected. RESULTS: After screening/selection 38 articles were included for a total of 114 patients. In our experience we selected 10 cases for a total of 16 IPTLs; 8 out of 10 patients underwent at least 1 MRI follow-up. Some reproducible and rather typical imaging findings for IPTL were found. The targetoid aspect of IPTL is very frequent in our experience (75% on T1W, 44% on T2W, 81% on contrast-enhanced T1W (at least one phase), 100% on Diffusion-W images) but is also recurrent in the literature (6% on T1W, 31% on T2W, 51% on CE-T1W (at least one phase), 18% on Diffusion-W images, and 67% on hepatobiliary phase). In our experience, Apparent Diffusion Coefficient map values were always equal to or higher than those of the surrounding parenchyma, and at MRI follow-up, nodule/s disappeared at first/second control, in six patients, while in the remaining 2, lesions persisted with tendency to dehydration. CONCLUSION: A targetoid-like aspect of a focal liver lesion must raise diagnostic suspicion, especially if IgG4-positive plasma is detected. MRI follow-up mainly shows the disappearance of the lesion or its reduction with dehydration.

Arterial hypertension and cystatin C during neonatal physiologic dehydration.

A reduced nephron number may play a role in the pathogenesis of arterial hypertension (AH), and it is well recognized that individual nephron endowment is widely variable. However, nephrons count is technically impossible in vivo. Based on the observation that subjects with a reduced nephron mass exhibit an increase in renal functional biomarkers during acute dehydration, we hypothesized that cystatin C concentration during neonatal physiological dehydration could identify subjects with reduced nephron endowment. This is a prospective, observational, cohort study enrolling healthy, caucasian, term neonates born after an uneventful pregnancy. Two groups of newborns were compared: neonates born to fathers on antihypertensive treatment (HF) versus those born to proven normotensive fathers older than 40 years of age (NF). Enrolled newborns underwent cystatin C determination at the time of newborn screening. Forty newborns with HF and 80 with NF were enrolled. No differences in baseline characteristics were observed between the two groups except for the number of hypertensive grandparents higher among newborns to HF (47.8% vs. 21.1%; p: 0.001). Cystatin C was significantly higher in newborns with HF (1.62 ± 0.30 mg/L vs 1.41 ± 0.27 mg/L; p < 0.001). Linear regression analysis corrected for confounders confirmed that paternal hypertension was the only variable significantly associated with high cystatin C level during post-natal dehydration. Besides offering new insights on the pathogenesis of familial hypertension, our results support the specific role of nephron endowment and suggest the possibility of identifying subjects at risk for reduced nephron endowment as early as at birth.

[Observing the time course of early long pyramidal tract Wallerian degeneration after acute ischemic stroke: a case report].

A 75-year-old man was found lying prostrate in a hot room in the middle of summer. On admission, he had high fever, dehydration, and multiple decubitus, in addition to right hemiparesis and total aphasia. Brain CT showed subacute ischemic stroke in the territory of left middle cerebral artery. Brain MRI diffusion-weighted imaging (DWI) 4 days after admission detected high signal intensity lesions in the left pyramidal tract from the midbrain cerebral peduncle to the lower pons, indicating early Wallerian degeneration. The lesions were found to extend to the contralateral pyramidal decussation by MRI DWI day 12, but they had disappeared on day 28. On the other hand, brain MRI FLAIR images detected the lesions clearly day 44. Also, diffusion tensor tractography detects fewer left cerebral pyramidal tracts. No previous reports have documented the time course of such long Wallerian degeneration. This case suggests that dehydration may promote the onset of early and long Wallerian degeneration.

Insights from a vertebrate model organism on the molecular mechanisms of whole-body dehydration tolerance.

Studies on the molecular mechanisms of dehydration tolerance have been largely limited to plants and invertebrates. Currently, research in whole body dehydration of complex animals is limited to cognitive and behavioral effects in humans, leaving the molecular mechanisms of vertebrate dehydration relatively unexplored. The present review summarizes studies to date on the African clawed frog (Xenopus laevis) and examines whole-body dehydration on physiological, cellular and molecular levels. This aquatic frog is exposed to seasonal droughts in its native habitat and can endure a loss of over 30% of its total body water. When coping with dehydration, osmoregulatory processes prioritize water retention in skeletal tissues and vital organs over plasma volume. Although systemic blood circulation is maintained in the vital organs and even elevated in the brain during dehydration, it is done so at the expense of reduced circulation to the skeletal muscles. Increased hemoglobin affinity for oxygen helps to counteract impaired blood circulation and metabolic enzymes show altered kinetic and regulatory parameters that support the use of anaerobic glycolysis. Recent studies with X. laevis also show that pro-survival pathways such as antioxidant defenses and heat shock proteins are activated in an organ-specific manner during dehydration. These pathways are tightly coordinated at the post-transcriptional level by non-coding RNAs, and at the post-translational level by reversible protein phosphorylation. Paired with ongoing research on the X. laevis genome, the African clawed frog is poised to be an ideal animal model with which to investigate the molecular adaptations for dehydration tolerance much more deeply.

The effect of religious fasting and dehydration at Ramadan on choroidal thickness and Retinal vessel densities, measured with optical coherence tomography angiography.

AIM: To investigate the effect of religious fasting and dehydration at Ramadan on choroidal thickness and vessel density in the superficial and deep vascular plexuses with OCTA. METHODS: The choroidal thickness, and superficial and deep vessel density indices of fasting healthy subjects were measured with an OCTA device, and compared with non-fasting measurements. RESULTS: The study included 70 eyes of 35 healthy subjects with a mean age of 42.86 ± 8.3 years. The measured choroidal thickness, superficial vessel density index and deep vessel density index were 288.89 ± 67 µm, 40.56% and 41.43%, respectively when measured in the fasting period, compared to 284.62 ± 65 µm, 40.41% and 41.41%, respectively when measured in the non-fasting period. The choroidal thickness under the fovea center was found to be significantly higher in the fasting period than in the non-fasting period (p = 0.014). The mean total choroidal thickness was found to be reduced in the non-fasting period, although not to a statistically significant degree (p > 0.05). An analysis of the mean total superficial and deep vascular plexuses revealed no statistically significant difference (p = 0.368, p = 0.938 respectively). CONCLUSION: Although a significant increase was noted in central choroidal thickness in the fasting period, no significant change due to fasting was observed in the superficial and deep capillary plexuses. The choroidal layer may vary in thickness due to fasting-related metabolic factors, while retinal vessels are more stable against such effects.

Fluid Intake Restriction Concomitant to Sweetened Beverages Hydration Induce Kidney Damage.

Currently, there is the paradox of low water intake but increased intake of sugar-sweetened beverages (SB) in several populations; those habits are associated with an increased prevalence of metabolic derangements and greater chronic disease mortality. Persistent heat dehydration and increased SB intake stimulate the continued release of vasopressin and overactivation of the polyol-fructokinase pathway, synergizing each other, an effect partially mediated by oxidative stress. The objective of the present study was to evaluate whether water restriction concurrent with SB hydration can cause renal damage by stimulating similar pathways as heat dehydration. Three groups of male Wistar rats (n = 6) were fluid restricted; from 10 am to 12 pm animals could rehydrate with tap water (W), or sweetened beverages, one prepared with 11% of a fructose-glucose combination (SB), or with the noncaloric edulcorant stevia (ST). A normal control group of healthy rats was also studied. The animals were followed for 4 weeks. Markers of dehydration and renal damage were evaluated at the end of the study. Fluid restriction and water hydration mildly increased urine osmolality and induced a 15% fall in CrCl while increased the markers of tubular damage by NAG and KIM-1. Such changes were in association with a mild overexpression of V1a and V2 renal receptors, polyol fructokinase pathway overactivation, and increased renal oxidative stress with reduced expression of antioxidant enzymes. Hydration with SB significantly amplified those alterations, while in stevia hydrated rats, the changes were similar to the ones observed in water hydrated rats. These data suggest that current habits of hydration could be a risk factor in developing kidney damage.

Seed Priming: A Feasible Strategy to Enhance Drought Tolerance in Crop Plants.

Drought is a serious threat to the farming community, biasing the crop productivity in arid and semi-arid regions of the world. Drought adversely affects seed germination, plant growth, and development via non-normal physiological processes. Plants generally acclimatize to drought stress through various tolerance mechanisms, but the changes in global climate and modern agricultural systems have further worsened the crop productivity. In order to increase the production and productivity, several strategies such as the breeding of tolerant varieties and exogenous application of growth regulators, osmoprotectants, and plant mineral nutrients are followed to mitigate the effects of drought stress. Nevertheless, the complex nature of drought stress makes these strategies ineffective in benefiting the farming community. Seed priming is an alternative, low-cost, and feasible technique, which can improve drought stress tolerance through enhanced and advanced seed germination. Primed seeds can retain the memory of previous stress and enable protection against oxidative stress through earlier activation of the cellular defense mechanism, reduced imbibition time, upsurge of germination promoters, and osmotic regulation. However, a better understanding of the metabolic events during the priming treatment is needed to use this technology in a more efficient way. Interestingly, the review highlights the morphological, physiological, biochemical, and molecular responses of seed priming for enhancing the drought tolerance in crop plants. Furthermore, the challenges and opportunities associated with various priming methods are also addressed side-by-side to enable the use of this simple and cost-efficient technique in a more efficient manner.

Unraveling the molecular pathobiology of vocal fold systemic dehydration using an in vivo rabbit model.

Vocal folds are a viscoelastic multilayered structure responsible for voice production. Vocal fold epithelial damage may weaken the protection of deeper layers of lamina propria and thyroarytenoid muscle and impair voice production. Systemic dehydration can adversely affect vocal function by creating suboptimal biomechanical conditions for vocal fold vibration. However, the molecular pathobiology of systemically dehydrated vocal folds is poorly understood. We used an in vivo rabbit model to investigate the complete gene expression profile of systemically dehydrated vocal folds. The RNA-Seq based transcriptome revealed 203 differentially expressed (DE) vocal fold genes due to systemic dehydration. Interestingly, function enrichment analysis showed downregulation of genes involved in cell adhesion, cell junction, inflammation, and upregulation of genes involved in cell proliferation. RT-qPCR validation was performed for a subset of DE genes and confirmed the downregulation of DSG1, CDH3, NECTIN1, SDC1, S100A9, SPINK5, ECM1, IL1A, and IL36A genes. In addition, the upregulation of the transcription factor NR4A3 gene involved in epithelial cell proliferation was validated. Taken together, these results suggest an alteration of the vocal fold epithelial barrier independent of inflammation, which could indicate a disruption and remodeling of the epithelial barrier integrity. This transcriptome provides a first global picture of the molecular changes in vocal fold tissue in response to systemic dehydration. The alterations observed at the transcriptional level help to understand the pathobiology of dehydration in voice function and highlight the benefits of hydration in voice therapy.

In Vivo Magnetic Resonance Imaging of the Rat Vocal Folds After Systemic Dehydration and Rehydration.

Objective Consuming less water (systemic dehydration) has long been thought to dehydrate the vocal folds. An in vivo, repeated measures study tested the assumption that systemic dehydration causes vocal fold dehydration. Proton density (PD)-weighted magnetic resonance imaging (MRI) of rat vocal folds was employed to investigate (a) whether varying magnitudes of systemic dehydration would dehydrate the vocal folds and (b) whether systemic rehydration would rehydrate the vocal folds. Method Male (n = 25) and female (n = 14) Sprague Dawley rats were imaged with 7T MRI, and normalized PD-weighted signal intensities were obtained at predehydration, following dehydration, and following rehydration. Animals were dehydrated to 1 of 3 levels by water withholding to induce body weight loss: mild (< 6% body weight loss), moderate (6%-10% body weight loss), and marked (> 10% body weight loss). Results There was a significant decrease in vocal fold signal intensities after moderate and marked dehydration (p < .0167). Rehydration increased the normalized signal intensity to predehydration levels for only the moderate group (p < .0167). Normalized signal intensity did not significantly change after mild dehydration or when the mildly dehydrated animals were rehydrated. Additionally, there were no significant differences in PD-weighted MRI normalized signal intensity between male and female rats (p > .05). Conclusion This study provides evidence supporting clinical voice recommendations for rehydration by increasing water intake after an acute, moderate systemic dehydration event. However, acute systemic dehydration of mild levels did not dehydrate the vocal folds as observed by PD-weighted MRI. Future programmatic research will focus on chronic, recurring systemic dehydration.

Gastroenteritis aggressive versus slow treatment for rehydration (GASTRO): a phase II rehydration trial for severe dehydration: WHO plan C versus slow rehydration.

BACKGROUND: World Health Organization rehydration management guidelines (plan C) for severe dehydration are widely practiced in resource-poor settings, but never formally evaluated in a trial. The Fluid Expansion as a Supportive Therapy trial raised concerns regarding the safety of bolus therapy for septic shock, warranting a formal evaluation of rehydration therapy for gastroenteritis. METHODS: A multi-centre open-label phase II randomised controlled trial evaluated two rehydration strategies in 122 Ugandan/Kenyan children aged 60 days to 12 years with severe dehydration secondary to gastroenteritis. We compared the safety and efficacy of standard rapid rehydration using Ringer's lactate (100 ml/kg over 3 h (6 h if < 1 year), incorporating 0.9% saline boluses for children with shock (plan C) versus slower rehydration: 100 ml/kg Ringer's lactate over 8 h (all ages) without boluses (slow: experimental). The primary outcome was the frequency of serious adverse events (SAE) within 48 h including cardiovascular, respiratory and neurological complications. Secondary outcomes included clinical, biochemical and physiological measures of response to treatment by intravenous rehydration. RESULTS: One hundred twenty-two eligible children (median (IQR) age 8 (6-12) months) were randomised to plan C (n = 61) or slow (n = 61), with two (2%) lost to follow-up at day 7). Following randomisation mean (SD) time to start intravenous rehydration started was 15 min (18) in both arms. Mean (SD) fluid received by 1 hour was greater in plan C (mean 20.2 ml/kg (12.2) and 33.1 ml/kg (17) for children < 1 year and >- 1 year respectively) versus 10.4 ml/kg (6.6) in slow arm. By 8 hours volume received were similar mean (SD) plan C: 96.3 ml/kg (15.6) and 97.8 ml/kg (10.0) for children < 1 and ≥ 1 year respectively vs 93.2 ml/kg (12.2) in slow arm. By 48-h, three (5%) plan C vs two (3%) slow had an SAE (risk ratio 0.67, 95% CI 0.12-3.85, p = 0.65). There was no difference in time to the correction of dehydration (p = 0.9) or time to discharge (p = 0.8) between groups. Atrial natriuretic peptide levels rose substantially by 8 hours in both arms, which persisted to day 7. Day 7 weights suggested only 33 (29%) could be retrospectively classified as severely dehydration (≥ 10% weight loss). CONCLUSION: Slower rehydration over 8 hours appears to be safe, easier to implement than plan C. Future large trials with mortality as the primary endpoint are warranted. TRIAL REGISTRATION: ISRCTN67518332 . Date applied 31 August 2016.

Effects of dehydration on echocardiographic diastolic parameters in healthy cats.

This study aimed to assess the effects of dehydration on echocardiographic indices in healthy cats: specifically, it aimed to assess the effects of volume depletion on diastolic function. Nine experimental cats were subjected to both a dehydration and placebo protocol separated by a 21-day washout period. Echocardiography was performed at baseline and on completion of each protocol. Results were compared between the two protocols. Volume depletion was induced by intravenous administration of furosemide. Volume depletion showed a significant association with increased interventricular septal and left ventricular free wall thickness at end-diastole, decreased left ventricular internal diameter at end-diastole, and left atrial diameter at end-systole. The peak early (E) and late (A) diastolic filling velocities, and the peak early diastolic velocities (E') were significantly decreased by dehydration. Volume depletion did not affect peak longitudinal strain rate during early diastole, E/A, or E/E'. Volume depletion significantly affected the echocardiographic diastolic indices and conventional echocardiographic parameters in healthy cats.

Dehydration and insulinopenia are necessary and sufficient for euglycemic ketoacidosis in SGLT2 inhibitor-treated rats.

Sodium-glucose transport protein 2 (SGLT2) inhibitors are a class of anti-diabetic agents; however, concerns have been raised about their potential to induce euglycemic ketoacidosis and to increase both glucose production and glucagon secretion. The mechanisms behind these alterations are unknown. Here we show that the SGLT2 inhibitor (SGLT2i) dapagliflozin promotes ketoacidosis in both healthy and type 2 diabetic rats in the setting of insulinopenia through increased plasma catecholamine and corticosterone concentrations secondary to volume depletion. These derangements increase white adipose tissue (WAT) lipolysis and hepatic acetyl-CoA content, rates of hepatic glucose production, and hepatic ketogenesis. Treatment with a loop diuretic, furosemide, under insulinopenic conditions replicates the effect of dapagliflozin and causes ketoacidosis. Furthermore, the effects of SGLT2 inhibition to promote ketoacidosis are independent from hyperglucagonemia. Taken together these data in rats identify the combination of insulinopenia and dehydration as a potential target to prevent euglycemic ketoacidosis associated with SGLT2i.

The effect of voluntary fasting and dehydration on posterior ocular structures.

PURPOSE: Islamic Ramadan is the month of fasting, in which intake of food and drink is restricted from sunrise until sunset. The objective of the present study was to find out the effects of religious fasting on posterior ocular structures. MATERIALS AND METHODS: In this prospective study, 34 eyes of 34 healthy volunteers with a mean age of 34.09 ± 7.20 years were enrolled. Volunteers with any systemic disorder and eyes with pathology or previous surgery were excluded. One week before Ramadan (non-fasting period) and during Ramadan (fasting period) at the same hours (at 08:00 and 16:00 h), choroidal, macular, and retinal nerve fibre layer (RNFL) thicknesses were measured by spectral domain optical coherence tomography. Results were compared using paired sample t-test, and a p value <0.05 was accepted as statistically significant. RESULTS: The comparison of 16:00-h measurements significantly revealed lower values during fasting period when compared non-fasting period for choroidal thickness (non-fasting and fasting, respectively; subfoveal: 299.26 ± 41.3 and 280.03 ± 38.75 p < 0.001, nasal: 246.09 ± 53.59 and 227.06 ± 53.82 p < 0.001, and temporal: 273.56 ± 42.68 and 257.44 ± 45.06 p = 0.001) and paracentral macular thickness (superior: p = 0.002, inferior: p = 0.010, temporal: p = 0.013, and nasal: p = 0.016). By contrast, no significant differences were found in the central macular thickness between the fasting and non-fasting periods (p = 0.735). Also, no statistically significant difference was noted for RNFL thickness at the different periods and time points. CONCLUSION: Our results reveal that Islamic religious fasting is associated with statistically significant alterations in choroidal and paracentral macular thickness in healthy volunteers. However, more detailed investigations should be designed to evaluate whether fasting has a pivotal influence on pathological conditions.

Narrative Review of Hydration and Selected Health Outcomes in the General Population.

Although adequate hydration is essential for health, little attention has been paid to the effects of hydration among the generally healthy population. This narrative review presents the state of the science on the role of hydration in health in the general population, specifically in skin health, neurological function (i.e., cognition, mood, and headache), gastrointestinal and renal functions, and body weight and composition. There is a growing body of evidence that supports the importance of adequate hydration in maintaining proper health, especially with regard to cognition, kidney stone risk, and weight management. However, the evidence is largely associative and lacks consistency, and the number of randomized trials is limited. Additionally, there are major gaps in knowledge related to health outcomes due to small variations in hydration status, the influence of sex and sex hormones, and age, especially in older adults and children.

Effects of long-term dehydration on oxidative stress, apoptotic markers and neuropeptides in the gastric mucosa of the dromedary camel.

We investigated the effects of 20 days of dehydration and 20 days of dehydration followed by 72 h of rehydration on the gastric mucosa of the one-humped dromedary camel. The parameters addressed include biomarkers of oxidative stress, apoptosis, gastric epithelial histology, gastric neuropeptides, and their receptors. Nineteen clinically healthy, 4-5 year-old male dromedary camels were divided into three groups (five control camels, eight dehydrated for 20 days, six dehydrated for 20 days and then rehydrated for 72 h). Dehydration affected the oxidative stress biomarkers causing a significant increase in malondialdehyde, glutathione, nitric oxide, and catalase values compared with controls. Also the results revealed that dehydration caused different size cellular vacuoles and focal necrosis in the gastric mucosa. Rehydration for 72 h resulted in improvement in some parameters but was not enough to fully abolish the effect of dehydration. Dehydration caused significant increase in apoptotic markers; tumor necrosis factor α, caspases 8 and 3, BcL-x1 and TGFß whereas caspase 9, p53, Beclin 1, and PARP1 showed no significant change between the three groups indicating that apoptosis was initiated by the extrinsic pathway. Also there were significant increases in prostaglandin E2 receptors and somatostatin in plasma and gastric epithelium homogenate, and a significant decrease in cholecystokinin-8 receptors. A significant decrease of hydrogen potassium ATPase enzyme activity was also observed. Pepsinogen C was not affected by dehydration. It is concluded that long-term dehydration induces oxidative stress and apoptosis in camel gastric mucosa and that camels adjust gastric functions during dehydration towards water economy. More than 72 h are needed before all the effects of dehydration are reversed by rehydration.