Paradoxical sleep deprivation induces oxidative stress in the submandibular glands of Wistar rats

Abstract

Objectives Paradoxical sleep deprivation has been associated with impaired salivary secretion in rats. However, the mechanism that underlies this is not known. Therefore, this study assessed salivary and serum oxidative stress levels following paradoxical sleep deprivation in rats. Methods Twenty-one male Wistar rats randomly divided into three groups of seven rats each as; Control (C); partial sleep-deprived (PSD); and total sleep-deprived (TSD) were used. Malondialdehyde (MDA) concentration, Superoxide dismutase (SOD), and catalase activities were evaluated in saliva, serum, and submandibular glands after seven days of sleep deprivation. Data were expressed as mean ± standard error of the mean and analyzed using one-way ANOVA, Tukey HSD post hoc, and Pearson’s correlation tests. Results Serum MDA levels were significantly higher in both the TSD and PSD groups compared to the control group whereas only the TSD group showed higher submandibular MDA levels compared to the PSD group and the control group. Submandibular SOD activity was significantly lower in both the TSD and PSD groups compared to the control group. Serum catalase activity was significantly lower in the TSD group only compared to the control group. Conclusions These results have demonstrated for the first time that paradoxical sleep deprivation was associated with changes in the oxidant/antioxidant defense system in the submandibular salivary glands of male Wistar rats which may contribute to impairment in salivary secretion.

Melatonin upregulates BMAL1 to attenuate chronic sleep deprivation‐related cognitive impairment by alleviating oxidative stress

“…MDA is a product of lipid peroxidation of polyunsaturated fatty acids by ROS, which reacts with various molecules (e.g., proteins, nucleosides, DNA, etc.) and may produce many adducts that promote cellular damage, and even lead to DNA mutation and induction of apoptosis (Lasisi et al., 2021 ). SOD is a key antioxidant enzyme that scavenges excess ROS and MDA, and its activity indirectly reflects the ability to scavenge oxygen radicals, and its reduced activity indicates antioxidant barrier damage.…”

Sleep Deprivation-Induced Oxidative Stress in Rat Models: A Scoping Systematic Review

“…As previously observed [ 9 ], the evidence from the included studies seems to point to changes in oxidative stress parameters in both brain (whole brain, hippocampus, cortex, thalamus, hypothalamus, amygdala, locus coeruleus) and non-brain areas (serum, testes, epididymis, liver, pancreas, aorta, submandibular glands, thyroid, erythrocytes, soleus muscle). However, some body sites did not show changes in oxidative stress parameters: cerebellum and brainstem [ 26 ], saliva [ 66 ], kidney [ 45 ], and plantar muscle [ 37 ]. While the evidence is limited in some cases, these observations might suggest that the antioxidant effects of sleep extend beyond the central nervous system, possibly including most body sites.…”

The role of sleep deprivation in physiological system dysfunctions

“…[85] also found that intestinal inflammation was triggered by an increase in proinflammatory cytokine levels in mice with sleep deprivation and that there was a decrease in gene expressions effective in the connections between the brain and the intestine, and as a result of these effects, intestinal permeability decreased. It has been found that the oxidative stress resulting from the disruption of oxidant/antioxidant balance in rats with paradoxical sleep deprivation leads to salivary secretion disorders [86]. According to Shigiyama et al [87], mice subjected to a 6-hour sleep deficiency period may develop hepatic steatosis and hepatic insulin resistance, with an increase in the levels of hepatic lipogenic enzymes perhaps acting as the underlying mechanism.…”