scholarly journals Heat and dehydration induced oxidative damage and antioxidant defenses following incubator heat stress and a simulated heat wave in wild caught four-striped field mice Rhabdomys dilectus

PLoS ONE ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. e0242279
Author(s):  
Paul J. Jacobs ◽  
M. K. Oosthuizen ◽  
C. Mitchell ◽  
Jonathan D. Blount ◽  
Nigel C. Bennett
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Heat Stress ◽  
Oxidative Damage ◽  
Heat Wave ◽  
Body Mass ◽  
Heat Waves ◽  
Heat Exposure ◽  
Field Mice ◽  
The Brain

Heat waves are known for their disastrous mass die-off effects due to dehydration and cell damage, but little is known about the non-lethal consequences of surviving severe heat exposure. Severe heat exposure can cause oxidative stress which can have negative consequences on animal cognition, reproduction and life expectancy. We investigated the current oxidative stress experienced by a mesic mouse species, the four striped field mouse, Rhabdomys dilectus through a heat wave simulation with ad lib water and a more severe temperature exposure with minimal water. Wild four striped field mice were caught between 2017 and 2019. We predicted that wild four striped field mice in the heat wave simulation would show less susceptibility to oxidative stress as compared to a more severe heat stress which is likely to occur in the future. Oxidative stress was determined in the liver, kidney and brain using malondialdehyde (MDA) and protein carbonyl (PC) as markers for oxidative damage, and superoxide dismutase (SOD) and total antioxidant capacity (TAC) as markers of antioxidant defense. Incubator heat stress was brought about by increasing the body temperatures of animals to 39–40.8°C for 6 hours. A heat wave (one hot day, followed by a 3-day heatwave) was simulated by using temperature cycle that wild four striped field mice would experience in their local habitat (determined through weather station data using temperature and humidity), with maximal ambient temperature of 39°C. The liver and kidney demonstrated no changes in the simulated heat wave, but the liver had significantly higher SOD activity and the kidney had significantly higher lipid peroxidation in the incubator experiment. Dehydration significantly contributed to the increase of these markers, as is evident from the decrease in body mass after the experiment. The brain only showed significantly higher lipid peroxidation following the simulated heat wave with no significant changes following the incubator experiment. The significant increase in lipid peroxidation was not correlated to body mass after the experiment. The magnitude and duration of heat stress, in conjunction with dehydration, played a critical role in the oxidative stress experienced by each tissue, with the results demonstrating the importance of measuring multiple tissues to determine the physiological state of an animal. Current heat waves in this species have the potential of causing oxidative stress in the brain with future heat waves to possibly stress the kidney and liver depending on the hydration state of animals.

Pyrroloquinoline quinone ameliorates oxidative stress and lipid peroxidation in the brain of streptozotocin-induced diabetic mice

2015 ◽  
Vol 93 (1) ◽  
pp. 71-79 ◽  
Author(s):  
Narendra Kumar ◽  
Anand Kar
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Body Mass ◽  
Serum Levels ◽  
Diabetic Mouse ◽  
Pyrroloquinoline Quinone ◽  
Oxygen Species ◽  
Diabetic Mice ◽  
The Brain

Diabetes, characterized by hyperglycemia, leads to several complications through the generation of reactive oxygen species and initiates tissue damage. Pyrroloquinoline quinone (PQQ) is believed to be a strong antioxidant, as it protects cells from oxidative damage. In this study, we elucidated the hitherto unknown potential of PQQ to ameliorate the brain damage caused by diabetes mellitus and the associated hyperglycemia-induced oxidative damage. Administration of a single dose of streptozotocin (STZ), i.e., 150 mg·(kg body mass)−1significantly enhanced the brain tissue levels of lipid peroxidation and hydroperoxidation and decreased the levels of antioxidants. It also increased the serum levels of glucose, cholesterol, and triglycerides. However, when STZ-treated animals received PQQ (20 mg·(kg body mass)−1·d−1, for 15 days), this significantly decreased the serum levels of glucose and lipid peroxidation products, and increased the activities of antioxidants in the diabetic mouse brain. These findings suggest that PQQ has the potential to ameliorate STZ-induced oxidative damage in the brain, as well as the STZ-induced diabetes.

scholarly journals Curcumin Reduce Sodium Fluoride-Induced Oxidative Stress in Rat Brain

2018 ◽  
Vol 15 (1) ◽  
pp. 71-77 ◽  
Author(s):  
Nagapuri Kiran Kumar ◽  
Mesram Nageshwar ◽  
Karnati Pratap Reddy
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Oral Administration ◽  
Rat Brain ◽  
Sodium Fluoride ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
The Brain

This study reports the ameliorative role of curcumin against sodium fluoride (NaF) induced oxidative stress in the brain of rats. The rats were divided into control, NaF (20 mg/kg), NaF+Curcumin (20mg/kg) and Curcumin (20mg/kg) groups respectively and treated at everyday interval for 60 consecutive days. Oxidative stress markers in the brain were measured at 60th day. NaF treatment significantly increased LPO content, but decreased the level of GSH and activities of SOD, GPx, and CAT the brain of rats in comparison to the control rats. Oral administration of curcumin to fluoride exposed rats significantly reversed the content of lipid peroxidation, as well as enhanced the level of GSH and SOD, GPx and CAT activities to normal compared to NaF exposed rats. Thus, curcumin showed the potential to prevent sodium fluoride induced oxidative damage in the brain of rats and curcumin may be useful agents against neurodegeneration in the brain.

Changes in lipid peroxidation during pregnancy and after delivery in rats: effect of pinealectomy

Reproduction ◽  
2000 ◽  
pp. 143-149 ◽  
Author(s):  
RM Sainz ◽  
RJ Reiter ◽  
JC Mayo ◽  
J Cabrera ◽  
DX Tan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Energy Demand ◽  
Physiological State ◽  
High Energy ◽  
Free Radical Scavengers ◽  
Radical Scavengers ◽  
Oxygen Requirement ◽  
Pregnant Rats

Pregnancy is a physiological state accompanied by a high energy demand of many bodily functions and an increased oxygen requirement. Because of the increased intake and utilization of oxygen, increased levels of oxidative stress would be expected. In the present study, the degree of lipid peroxidation was examined in different tissues from non-pregnant and pregnant rats after the delivery of their young. Melatonin and other indole metabolites are known to be direct free radical scavengers and indirect antioxidants. Thus the effect of pinealectomy at 1 month before pregnancy on the accumulation of lipid damage was investigated in non-pregnant and pregnant rats after the delivery of their young. Malonaldehyde and 4-hydroxyalkenal concentrations were measured in the lung, uterus, liver, brain, kidney, thymus and spleen from intact and pinealectomized pregnant rats soon after birth of their young and at 14 and 21 days after delivery. The same parameters were also evaluated in intact and pinealectomized non-pregnant rats. Shortly after delivery, lipid oxidative damage was increased in lung, uterus, brain, kidney and thymus of the mothers. No differences were detected in liver and spleen. Pinealectomy enhanced this effect in the uterus and lung. It is concluded that during pregnancy high levels of oxidative stress induce an increase in oxidative damage to lipids, which in some cases is inhibited by the antioxidative actions of pineal indoles.

scholarly journals Mn Inhibits GSH Synthesis via Downregulation of Neuronal EAAC1 and Astrocytic xCT to Cause Oxidative Damage in the Striatum of Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
Xinxin Yang ◽  
Haibo Yang ◽  
Fengdi Wu ◽  
Zhipeng Qi ◽  
Jiashuo Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Dependent Manner ◽  
Protein Levels ◽  
Key Factor ◽  
Protein Sulfhydryl ◽  
Mrna And Protein Expression ◽  
The Brain

Excessive manganese (Mn) can accumulate in the striatum of the brain following overexposure. Oxidative stress is a well-recognized mechanism in Mn-induced neurotoxicity. It has been proven that glutathione (GSH) depletion is a key factor in oxidative damage during Mn exposure. However, no study has focused on the dysfunction of GSH synthesis-induced oxidative stress in the brain during Mn exposure. The objective of the present study was to explore the mechanism of Mn disruption of GSH synthesis via EAAC1 and xCT in vitro and in vivo. Primary neurons and astrocytes were cultured and treated with different doses of Mn to observe the state of cells and levels of GSH and reactive oxygen species (ROS) and measure mRNA and protein expression of EAAC1 and xCT. Mice were randomly divided into seven groups, which received saline, 12.5, 25, and 50 mg/kg MnCl2, 500 mg/kg AAH (EAAC1 inhibitor) + 50 mg/kg MnCl2, 75 mg/kg SSZ (xCT inhibitor) + 50 mg/kg MnCl2, and 100 mg/kg NAC (GSH rescuer) + 50 mg/kg MnCl2 once daily for two weeks. Then, levels of EAAC1, xCT, ROS, GSH, malondialdehyde (MDA), protein sulfhydryl, carbonyl, 8-hydroxy-2-deoxyguanosine (8-OHdG), and morphological and ultrastructural features in the striatum of mice were measured. Mn reduced protein levels, mRNA expression, and immunofluorescence intensity of EAAC1 and xCT. Mn also decreased the level of GSH, sulfhydryl, and increased ROS, MDA, 8-OHdG, and carbonyl in a dose-dependent manner. Injury-related pathological and ultrastructure changes in the striatum of mice were significantly present. In conclusion, excessive exposure to Mn disrupts GSH synthesis through inhibition of EAAC1 and xCT to trigger oxidative damage in the striatum.

scholarly journals C60 Fullerene Prevents Restraint Stress-Induced Oxidative Disorders in Rat Tissues: Possible Involvement of the Nrf2/ARE-Antioxidant Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-17 ◽  
Author(s):  
Olga O. Gonchar ◽  
Andriy V. Maznychenko ◽  
Nataliya V. Bulgakova ◽  
Inna V. Vereshchaka ◽  
Tomasz Tomiak ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Protein Expression ◽  
Restraint Stress ◽  
Stress Condition ◽  
Rat Tissues ◽  
Stress Exposure ◽  
The Brain ◽  
Nrf2 Protein

The effects of C60FAS (50 and 500 μg/kg) supplementation, in a normal physiological state and after restraint stress exposure, on prooxidant/antioxidant balance in rat tissues were explored and compared with the effects of the known exogenous antioxidant N-acetylcysteine. Oxidative stress biomarkers (ROS, O2⋅−, H2O2, and lipid peroxidation) and indices of antioxidant status (MnSOD, catalase, GPx, GST, γ-GCL, GR activities, and GSH level) were measured in the brain and the heart. In addition, protein expression of Nrf2 in the nuclear and cytosol fractions as well as the protein level of antiradical enzyme MnSOD and GSH-related enzymes γ-GCLC, GPx, and GSTP as downstream targets of Nrf2 was evaluated by western blot analysis. Under a stress condition, C60FAS attenuates ROS generation and O2⋅− and H2O2 releases and thus decreases lipid peroxidation as well as increases rat tissue antioxidant capacity. We have shown that C60FAS supplementation has dose-dependent and tissue-specific effects. C60FAS strengthened the antiradical defense through the upregulation of MnSOD in brain cells and maintained MnSOD protein content at the control level in the myocardium. Moreover, C60FAS enhanced the GSH level and the activity/protein expression of GSH-related enzymes. Correlation of these changes with Nrf2 protein content suggests that under stress exposure, along with other mechanisms, the Nrf2/ARE-antioxidant pathway may be involved in regulation of glutathione homeostasis. In our study, in an in vivo model, when C60FAS (50 and 500 μg/kg) was applied alone, no significant changes in Nrf2 protein expression as well as in activity/protein levels of MnSOD and GSH-related enzymes in both tissues types were observed. All these facts allow us to assume that in the in vivo model, C60FAS affects on the brain and heart endogenous antioxidative statuses only during the oxidative stress condition.

scholarly journals Using naturalistic incubation temperatures to demonstrate how variation in the timing and continuity of heat wave exposure influences phenotype

2020 ◽  
Vol 287 (1932) ◽  
pp. 20200992 ◽  
Author(s):  
Anthony T. Breitenbach ◽  
Amanda W. Carter ◽  
Ryan T. Paitz ◽  
Rachel M. Bowden
Keyword(s):  
Heat Wave ◽  
Time Course ◽  
Heat Waves ◽  
Heat Exposure ◽  
Effect Of Temperature ◽  
Similar Time ◽  
Expression Of Genes ◽  
Short Period ◽  
The Face ◽  
Temperature Exposure

Most organisms are exposed to bouts of warm temperatures during development, yet we know little about how variation in the timing and continuity of heat exposure influences biological processes. If heat waves increase in frequency and duration as predicted, it is necessary to understand how these bouts could affect thermally sensitive species, including reptiles with temperature-dependent sex determination (TSD). In a multi-year study using fluctuating temperatures, we exposed Trachemys scripta embryos to cooler, male-producing temperatures interspersed with warmer, female-producing temperatures (heat waves) that varied in either timing during development or continuity and then analysed resulting sex ratios. We also quantified the expression of genes involved in testis differentiation ( Dmrt1 ) and ovary differentiation ( Cyp19A1 ) to determine how heat wave continuity affects the expression of genes involved in sexual differentiation. Heat waves applied during the middle of development produced significantly more females compared to heat waves that occurred just 7 days before or after this window, and even short gaps in the continuity of a heat wave decreased the production of females. Continuous heat exposure resulted in increased Cyp19A1 expression while discontinuous heat exposure failed to increase expression in either gene over a similar time course. We report that even small differences in the timing and continuity of heat waves can result in drastically different phenotypic outcomes. This strong effect of temperature occurred despite the fact that embryos were exposed to the same number of warm days during a short period of time, which highlights the need to study temperature effects under more ecologically relevant conditions where temperatures may be elevated for only a few days at a time. In the face of a changing climate, the finding that subtle shifts in temperature exposure result in substantial effects on embryonic development becomes even more critical.

scholarly journals Strawberry Intake Ameliorates Oxidative Stress and Decreases GABA Levels Induced by High-Fat Diet in Frontal Cortex of Rats

Antioxidants ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 70 ◽  
Author(s):  
Cuauhtémoc Sandoval-Salazar ◽  
Cecilia Oviedo-Solís ◽  
Edmundo Lozoya-Gloria ◽  
Herlinda Aguilar-Zavala ◽  
Martha Solís-Ortiz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Frontal Cortex ◽  
Protein Oxidation ◽  
High Fat Diet ◽  
High Fat ◽  
Gaba Concentration ◽  
Obese Rats ◽  
Lipid And Protein Oxidation

It has been proposed that there is a correlation between high-fat diet (HFD), oxidative stress and decreased γ-aminobutyric acid (GABA) levels, but this has not been thoroughly demonstrated. In the present study, we determined the effects of strawberry extract intake on the oxidative stress and GABA levels in the frontal cortex (FC) of obese rats. We observed that an HFD increased lipid and protein oxidation, and decreased GABA levels. Moreover, UV-irradiated strawberry extract (UViSE) decreased lipid peroxidation but not protein oxidation, whereas non-irradiated strawberry extract (NSE) reduced protein oxidation but not lipid peroxidation. Interestingly, NSE increased GABA concentration, whereas UViSE was not as effective. In conclusion, our results suggest that an HFD increases oxidative damage in the FC, whereas strawberry extract intake may ameliorate the disturbances associated with HFD-induced oxidative damage.

scholarly journals O8B.6 Occupational heat stress due to climate change: estimating future heat wave hazards

2019 ◽  
Vol 76 (Suppl 1) ◽  
pp. A73.2-A73
Author(s):  
Matthias Otto ◽  
Tord Kjellstrom ◽  
Bruno Lemke
Keyword(s):  
Climate Change ◽  
Heat Stress ◽  
Occupational Health ◽  
Health Effects ◽  
Heat Wave ◽  
Climate Models ◽  
Heat Waves ◽  
Grid Cell ◽  
High Heat ◽  
Temperate Climate

Exposure to extreme heat negatively affects occupational health. Heat stress indices like Wet Bulb Globe Temperature (WBGT) combine temperature and humidity and allow quantifying the climatic impact on human physiology and clinical health. Multi-day periods of high heat stress (aka. heat waves) affect occupational health and productivity independently from the absolute temperature levels; e.g. well-documented heat-waves in Europe caused disruption, hospitalisations and deaths (2003 French heat wave: more than 1000 extra deaths, 15–65 years, mainly men) even though the temperatures were within the normal range of hotter countries.Climate change is likely to increase frequency and severity of periods of high heat stress. However, current global grid-cell based climate models are not designed to predict heat waves, neither in terms of severity or frequency.By analysing 37 years of historic daily heat index data from almost 5000 global weather stations and comparing them to widely used grid-cell based climate model outputs over the same period, our research explores methods to assess the frequency and intensity of heat waves as well as the associated occupational health effects at any location around the world in the future.Weather station temperature extreme values (WBGT) for the 3 hottest days in 30 years exceed the mean WBGT of the hottest month calculated from climate models in the same grid-cell by about 2 degrees in the tropics but by 10 degrees at higher latitudes in temperate climate regions.Our model based on the relationship between actual recorded periods of elevated heat-stress and grid-cell based climate projections, in combination with population and employment projections, can quantify national and regional productivity loss and health effects with greater certainty than is currently the case.

Acutely administered melatonin reduces oxidative damage in lung and brain induced by hyperbaric oxygen

1997 ◽  
Vol 83 (2) ◽  
pp. 354-358 ◽  
Author(s):  
Marta I. Pablos ◽  
Russel J. Reiter ◽  
Jin-Ing Chuang ◽  
Genaro G. Ortiz ◽  
Juan M. Guerrero ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Hyperbaric Oxygen ◽  
Antioxidative Enzymes ◽  
Melatonin Receptors ◽  
Cellular Damage ◽  
Oxygen Exposure ◽  
Glutathione Status ◽  
Hyperbaric Oxygen Exposure ◽  
The Brain

Pablos, Marta I., Russel J. Reiter, Jin-Ing Chuang, Genaro G. Ortiz, Juan M. Guerrero, Ewa Sewerynek, Maria T. Agapito, Daniela Melchiorri, Richard Lawrence, and Susan M. Deneke. Acutely administered melatonin reduces oxidative damage in lung and brain induced by hyperbaric oxygen. J. Appl. Physiol. 83(2): 354–358, 1997.—Hyperbaric oxygen exposure rapidly induces lipid peroxidation and cellular damage in a variety of organs. In this study, we demonstrate that the exposure of rats to 4 atmospheres of 100% oxygen for 90 min is associated with increased levels of lipid peroxidation products [malonaldehyde (MDA) and 4-hydroxyalkenals (4-HDA)] and with changes in the activities of two antioxidative enzymes [glutathione peroxidase (GPX) and glutathione reductase (GR)], as well as in the glutathione status in the lungs and in the brain. Products of lipid peroxidation increased after hyperbaric hyperoxia, both GPX and GR activities were decreased, and levels of total glutathione (reduced+oxidized) and glutathione disulfide (oxidized glutathione) increased in both lung and brain areas (cerebral cortex, hippocampus, hypothalamus, striatum, and cerebellum) but not in liver. When animals were injected with melatonin (10 mg/kg) immediately before the 90-min hyperbaric oxygen exposure, all measurements of oxidative damage were prevented and were similar to those in untreated control animals. Melatonin’s actions may be related to a variety of mechanisms, some of which remain to be identified, including its ability to directly scavenge free radicals and its induction of antioxidative enzymes via specific melatonin receptors.

Hepatoprotection by carotenoids in isoniazid–rifampicin induced hepatic injury in rats

2010 ◽  
Vol 88 (5) ◽  
pp. 819-834 ◽  
Author(s):  
S. V. Rana ◽  
R. Pal ◽  
K. Vaiphei ◽  
R. P. Ola ◽  
K. Singh
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Alkaline Phosphatase ◽  
Superoxide Dismutase ◽  
Body Mass ◽  
Hepatic Injury ◽  
Control Group ◽  
Adult Rats ◽  
Partial Protection ◽  
Phosphatase Treatment

This study evaluates the hepatoprotective effect of carotenoids against isoniazid (INH) and rifampicin (RIF). Thirty-six adult rats were divided into the following 4 groups: (1) control group treated with normal saline; (2) INH + RIF group treated with 50 mg·(kg body mass)–1·day–1 of INH and RIF each; (3) INH + RIF+ carotenoids group treated with 50 mg·(kg body mass)–1·day–1 of INH and RIF each and 10 mg·(kg body mass)–1·day–1 of carotenoids; and (4) carotenoids group treated with 10 mg·(kg body mass)–1·day–1 of carotenoids for 28 days intragastrically. Oxidative stress and antioxidant levels in liver and blood, liver histology and change in transaminases were measured in all the above-mentioned groups. There was an increase in lipid peroxidation with a reduction in thiols, catalase, and superoxide dismutase (SOD) in the liver and blood of rats accompanied by an increase in transaminases, bilirubin, and alkaline phosphatase. Treatment with carotenoids along with INH + RIF partially reversed lipid peroxidation, thiols, catalase, and SOD in the liver and blood of rats. Elevated levels of the enzymes in serum were also reversed partially by this treatment. The degree of necrosis, portal triaditis, and inflammation were also lowered in the carotenoids group. In conclusion, carotenoids supplementation in INH + RIF treated rats showed partial protection.

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