Abstract:Background: The aim of this study was to investigate ultrastructural and apoptotic changes occurring in the kidneys in fasting individuals and to examine the effects of histamine treatment at the electron-microscopic and immunohistochemical levels. Methods: Eighteen adult Wistar male rats were randomly divided into three groups (n=6 for each). Control group (1), fasting group (12 h) (2), and fasting+histamine injection (0.5 mg/kg) (3) group. Expression of caspase-3 and caspase-9 was determined in the tissue sections using immunohistochemical techniques. Quantitative data were obtained using H-SCORE, and statistical evaluations were then performed. The ultrastructure of the kidney tissues was examined using transmission electron microscopy. Results: Weak caspase-3 and caspase-9 expression was observed in the renal tubules and glomeruli in the control group, while immunoreactivity was more intense in the fasting group (p < 0.05). In the fasting+histamine group, caspase-3 and caspase-9 immunostaining was signifi cantly positive in both renal tubules and glomeruli (p <0.05). At electron microscopic evaluation, degenerative changes were seen in the glomeruli of the fasting group, as well as partial vacuolization and disruption at the basal foldings in the tubular epithelial cells. In the fasting+histamine group, in addition to signifi cant dilatation of all glomerular capillaries, there were degenerative changes in all tubular and canalicular epithelial cells in the proximal tubules. Conclusions: Fasting, an important metabolic stress factor, accompanied by histamine treatment may cause signifi cant disruptions in the kidneys, particularly in the glomerular capillaries and proximal and distal tubules (Tab. 1, Fig. 2 Acknowledgements: We confi rm that we have read the Journal's position on issues involved in ethical publication and affi rm that this report is consistent with those guidelines.

Introduction Hypoxia can occur due to natural causes, such as travel to or living in high altitudes, or it can occur because of pathological events such as ischemia, cardiac arrest, or blood loss. Neurons of the central nervous system are particularly sensitive to different forms of hypoxia because of their high metabolic demands and limited glucose storage capacity. Hypoxia/ischemia triggers a variety of processes that lead to changes in intracellular signal transduction, membrane function, metabolism, and even cell morphology [1,2]. These processes may cause cellular damage or death. Hypoxic or ischemic preconditioning (PC or IPC) is based on a phenomenon in which transient and mild hypoxia/ischemia set cells and increase cellular resistance against subsequent lethal ischemic/hypoxic injury. In recent years, several studies have shown the protective effects of PC/IPC on different organs such as the kidney, lung, and heart in both in vivo and in vitro experimental settings [3-7]. However, information on the underlying mechanisms of PC/IPC which provide protection against ischemic/hypoxic insults is limited, and still being investigated. Endogenous opioid peptides function as neurotransmitters or neuromodulators in the central nervous system and exert their effects via mu, delta, and kappa receptors (MOR, DOR, and KOR, respectively). These receptors are G protein-coupled receptors (GPCR) and are common in the central nervous system [8]. Several studies have shown that among all opioid receptors, DOR is the most sensitive to stressors like hypoxia/ischemia, and it may have a role in neuroprotective processes against hypoxic/ischemic stress [9]. DOR has been shown to be more abundant in the turtle brain than in the rat brain; concordant with this, neurons in turtle brain are much more resistant to hypoxic/ischemic stress [10,11]. DOR expression in the rat brain cortex is more prominent compared to subcortical areas such as the Background/aim: The purpose of the present study was to explore the neuroprotective role of delta opioid receptors (DOR) in the rat cortex in hypoxic preconditioning.