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

Author(s):  
Taye J. Lasisi ◽  
Shehu-Tijani T. Shittu ◽  
Jude I. Abeje ◽  
Kehinde J. Ogunremi ◽  
Seyyid A. Shittu

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.

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5567 ◽  
Author(s):  
Malinalli Brianza-Padilla ◽  
Fausto Sánchez-Muñoz ◽  
Gonzalo Vázquez-Palacios ◽  
Fengyang Huang ◽  
Julio César Almanza-Pérez ◽  
...  

Background Sleep has a fundamental role in the regulation of homeostasis. The aim of this study was to assess the effect of different periods of paradoxical sleep deprivation (PSD) and recovery on serum levels of cytokines and miRNAs related to inflammatory responses. Methods Male Wistar rats were submitted to a PSD of 24, 96, or 192 h, or of 192 h followed by 20 days of recovery (192 h PSD+R). The concentrations of corticosterone, cytokines (IL-6, TNF, IL-10, Adiponectin) and miRNAs (miR-146a, miR-155, miR-223, miR-16, miR-126, miR-21) in serum were evaluated. Results At PSD 24 h a significant increase of IL-6 and decrease of IL-10 were observed. At PSD 96h adiponectin increased. At 192 h of PSD IL-6 increased significantly again, accompanied by a threefold increase of IL-10 and an increase of serum corticosterone. After 20 days of recovery (192 h PSD+R) corticosterone, IL-6 and TNF levels increased significantly, while IL-10 decreased also significantly. Regarding the miRNAs at 24 h of PSD serum miR-146a, miR-155, miR-223, and miR-16 levels all increased. At 96 h of PSD miR-223 decreased. At 192 h of PSD decreases in miR-16 and miR-126 were observed. After recovery serum miR-21 increased and miR-16 decreased. Conclusion PSD induces a dynamic response likely reflecting the induced cellular stress and manifested as variating hormonal and inflammatory responses. Sleep deprivation disturbed corticosterone, cytokine and miRNA levels in serum related to the duration of sleep deprivation, as short-term PSD produced effects similar to those of an acute inflammatory response and long-term PSD induced long-lasting disturbances of biological mediators.


2016 ◽  
Vol 99 ◽  
pp. 79-86 ◽  
Author(s):  
Luiz K.S. Kanazawa ◽  
Débora D. Vecchia ◽  
Etiéli M. Wendler ◽  
Palloma de A.S. Hocayen ◽  
Francislaine A. dos Reis Lívero ◽  
...  

2015 ◽  
pp. 153-159 ◽  
Author(s):  
M. M. GOVENDER ◽  
A. NADAR

Oxidative stress is an imbalance between free radicals and antioxidants, and is an important etiological factor in the development of hypertension. Recent experimental evidence suggests that subpressor doses of angiotensin II elevate oxidative stress and blood pressure. We aimed to investigate the oxidative stress related mechanism by which a subpressor dose of angiotensin II induces hypertension in a normotensive rat model. Normotensive male Wistar rats were infused with a subpressor dose of angiotensin II for 28 days. The control group was sham operated and infused with saline only. Plasma angiotensin II and H2O2 levels, whole-blood glutathione peroxidase, and AT-1a, Cu/Zn SOD, and p22phox mRNA expression in the aorta was assessed. Systolic and diastolic blood pressures were elevated in the experimental group. There was no change in angiotensin II levels, but a significant increase in AT-1a mRNA expression was found in the experimental group. mRNA expression of p22phox was increased significantly and Cu/Zn SOD decreased significantly in the experimental group. There was no significant change to the H2O2 and GPx levels. Angiotensin II manipulates the free radical-antioxidant balance in the vasculature by selectively increasing O2− production and decreasing SOD activity and causes an oxidative stress induced elevation in blood pressure in the Wistar rat.


2014 ◽  
Vol 66 (3) ◽  
pp. 1075-1081
Author(s):  
Ivan Simic ◽  
Violeta Iric-Cupic ◽  
Rada Vucic ◽  
Marina Petrovic ◽  
Violeta Mladenovic ◽  
...  

The aim of the present study was to evaluate the subchronic effects of 3,4-methylenedioxymethamphetamine on several oxidative stress markers: index of lipid peroxidation (ILP), superoxide dismutase (SOD) activity, superoxide radical (O2.-) levels, and reduced glutathione (GSH) levels in the frontal cortex, striatum and hippocampus of the rat. The study included 64 male Wistar rats (200-250g). The animals were treated per os with of 5, 10, or 20 mg/kg of 3,4-methylenedioxymethamphetamine (MDMA) every day for 15 days. The subchronic administration of MDMA resulted in an increase in ILP, SOD and O2.-, and a decrease in GSH, from which we conclude that oxidative stress was induced in rat brain.


Author(s):  
Ayodeji J Ajibare ◽  
Olabode O Akintoye ◽  
Oyesanmi A Fabunmi ◽  
Luqman A Olayak ◽  
Babatunde A Olofinbiyi ◽  
...  

Background: Sleep deprivation is a public health problem that causes oxidative stress injury. Research evidence agrees that oxidative stress serves as an underlying factor in many chronic debilitating diseases. This study investigated the effect of aqueous Licorice extract (Glycyrrhiza glabra) a medicinal plant with known antioxidant activity on testicular oxidative stress parameters. Methods Twenty-five male Wistar rats were randomly allocated to and administered one of the following treatment regimens daily for five days: CONTROL – Distilled water, Sleep – Deprived (SD) – Distilled water, Sleep Deprived +Sleep Recovery (SD+SR) – Distilled Water, SD+LICORICE (SD+LICORICE) – 150 mg/kg bodyweight of Licorice and Sleep – Deprivation + Sleep-Recovery + Licorice (SD+SR+LICORICE) – 150 mg/kg bodyweight of Licorice. The rats in Sleep – Recovery groups were allowed to sleep in their cages after sleep deprivation protocol for 5 days each treatment regimen had ad libitum access to standard rat chow. After the experiment, the rats were sacrificed and blood was collected. Serum cortisol and testosterone were taken alongside testicular Glutathione, Catalase, and Malondialdehyde. Results Sleep deprivation significantly raised cortisol level and decreased testosterone levels both of which were reversed by licorice administration. Significant reduction in Malondialdehyde (MDA) in rats treated with licorice with a simultaneous increase in both GSH and CAT was also observed. Conclusions The antioxidant activity of licorice (Glycyrrhiza glabra) aqueous extract on the testis of rats exposed to oxidative stress suggests the potential of using this traditional medicinal plant in preventing oxidative injury caused by sleep deprivation.


PLoS ONE ◽  
2021 ◽  
Vol 16 (12) ◽  
pp. e0260546
Author(s):  
Mary J. Obayemi ◽  
Christopher O. Akintayo ◽  
Adesola A. Oniyide ◽  
Ayodeji Aturamu ◽  
Olabimpe C. Badejogbin ◽  
...  

Background Adipose and hepatic metabolic dysfunctions are critical comorbidities that also aggravate insulin resistance in obese individuals. Melatonin is a low-cost agent and previous studies suggest that its use may promote metabolic health. However, its effects on some comorbidities associated with obesity are unknown. Herein, we investigated the hypothesis that melatonin supplementation would attenuate adipose-hepatic metabolic dysfunction in high fat diet (HFD)-induced obesity in male Wistar rats. Materials and methods Twenty-four adult male Wistar rats (n = 6/group) were used: Control group received vehicle (normal saline), obese group received 40% high fat diet, melatonin-treated group received 4 mg/kg of melatonin, and obese plus melatonin group received 40% HFD and melatonin. The treatment lasted for 12 weeks. Results HFD caused increased food intake, body weight, insulin level, insulin resistance and plasma and liver lipid but decreased adipose lipid. In addition, HFD also increased plasma, adipose and liver malondialdehyde, IL-6, uric acid and decreased Glucose-6-phosphate dehydrogenase, glutathione, nitric oxide and circulating obestatin concentration. However, these deleterious effects except food intake were attenuated when supplemented with melatonin. Conclusion Taken together, the present results indicate that HFD exposure causes adipose-hepatic metabolic disturbance in obese animals, which are accompanied by oxidative stress and inflammation. In addition, the present results suggest that melatonin supplementation attenuates adipose-hepatic metabolic dysfunction, accompanying obesity by suppression of oxidative stress/inflammation-dependent mechanism and increasing circulating obestatin.


2014 ◽  
Vol 387 (5) ◽  
pp. 399-406 ◽  
Author(s):  
Alisson Menezes Araujo Lima ◽  
Veralice Meireles Sales de Bruin ◽  
Emiliano Ricardo Vasconcelos Rios ◽  
Pedro Felipe Carvalhedo de Bruin

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