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

Authors
  • Ali, Mahmoud A.1
  • Damir, Hassan Abu
  • Amir, Naheed1
  • Adeghate, E. A.2
  • Bastaki, Salim1
  • Murphy, David3
  • Adem, Abdu1
  • 1 United Arab Emirates University, Department of Pharmacology, College of Medicine and Health Sciences, Al-Ain, UAE , Al-Ain (United Arab Emirates)
  • 2 United Arab Emirates University, Department of Anatomy, College of Medicine and Health Sciences, Al-Ain, UAE , Al-Ain (United Arab Emirates)
  • 3 Bristol Medical School, Molecular Neuroendocrinology Research Laboratory, Translational Health Sciences, Dorothy Hodgkin Building, Bristol, UK , Bristol (United Kingdom)
Type
Published Article
Journal
Molecular and Cellular Biochemistry
Publisher
Springer-Verlag
Publication Date
Nov 26, 2018
Volume
455
Issue
1-2
Pages
109–118
Identifiers
DOI: 10.1007/s11010-018-3474-x
Source
Springer Nature
Keywords
License
Yellow

Abstract

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 TGFβ 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.

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