Oxidative Stress In Obese Rats Research Articles

Capsinoids Increase Antioxidative Enzyme Activity and Prevent Obesity-Induced Cardiac Injury without Positively Modulating Body Fat Accumulation and Cardiac Oxidative Biomarkers.

Capsinoids are potential antioxidant agents capable of reducing oxidative damage and the resulting complications triggered by obesity. Thus, this study aimed to investigate the effects of capsinoids on adiposity and biomarkers of cardiac oxidative stress in obese rats induced by a high-fat diet. Male Wistar rats were exposed to a high-fat diet for 27 consecutive weeks. After the characterization of obesity (week 19), some of the obese animals began to receive capsinoids (10 mg/kg/day) by orogastric gavage. Adiposity and comorbidities were assessed. In the heart, remodeling, injury, and biomarkers of oxidative stress were determined. The treatment did not reduce obesity-induced adiposity but was efficient in reducing cholesterol levels. Capsinoid treatment did not cause a difference in heart and LV mass, despite having reduced troponin I concentrations. Furthermore, capsinoids did not reduce the increase in the advanced oxidation of protein products and carbonylated proteins caused by obesity in cardiac tissue. In addition, obese rats treated with capsinoids presented high levels of malondialdehyde and greater antioxidant enzyme activity compared to untreated obese rats. In conclusion, treatment with capsinoids increases antioxidative enzyme activity and prevents obesity-induced cardiac injury without positively modulating body fat accumulation and cardiac oxidative biomarkers.

A MUFA/carotenoid-rich oil ameliorated insulin resistance by improving inflammation and oxidative stress in obese rats

Obesity is associated with low-grade inflammation and oxidative stress, leading to insulin resistance and type II diabetes. Caryocar brasiliense pulp oil (pequi oil – PO) is rich in oleic acid and carotenoids and positively implicated in regulating inflammation and oxidative stress. This study investigated PO's antioxidant and anti-inflammatory effects in a diet-induced obesity model. Male Wistar rats were allocated into three experimental groups: Control (CD), Western Diet (WD), and Western Diet, with 27% of lard switched by PO (WDP). Metabolic, inflammatory, and oxidative stress biomarkers were evaluated after 12 weeks of diet protocols in liver and adipose tissue. WDP rats gained less body mass and epididymal fat, had less hepatic fat infiltration, and were more glucose-tolerant and insulin-sensitive than WD (p < 0.05). In the liver, the WDP group had the highest non-enzymatic antioxidant capacity, SOD and GPx activities, CAT, SOD II, and HSP72 expression compared to WD (p < 0.05). Adipose tissue IL-6 and TNF were reduced, and IL-10 was increased in WDP compared to WD (p < 0.05). Our data suggest that the partial replacement of lard by PO in a Western diet prevented visceral fat accumulation and contributed to reducing inflammation in adipose tissue and liver oxidative stress, improving obesity-related insulin resistance.

Valorization of Encapsulated Coffee Parchment Extracts as Metabolic Control for High Fructose Diet-Induced Obesity, Using Wistar Rat as Animal Model

Parchment is a coffee by-product with high amounts of polyphenols that could be effective in the prevention of obesity-related metabolic disorders. However, their effectiveness depends on their stability and bioavailability which could be improved by encapsulation. The aim of this study was to investigate anti-obesity effects of aqueous coffee parchment extract. Aqueous coffee parchment extracts were administrated orally (100 mg/kg weight/day) as free or in a microencapsulated form with whey protein/maltodextrin, in fructose-induced obesity rat model (20% fructose in water). Different metabolic parameters were determined. Parchment extract contained total phenolics at 79.50 mg GAE/g, with chlorogenic acid and caffeine as main compounds. The microencapsulation efficiency was 89.36% and SEM images revealed spherical microcapsules which exhibited polyphenol release under simulated digestion. Fructose obese rats displayed increased adiposity and metabolic alterations as hyperinsulinemia, hyperglycemia, hyperlipidemia and oxidative stress with high liver and adipose tissue lipids. The treatment with parchment extract prevented adipose fat accumulation and alleviated the hyperglycemia, hyperinsulinemia, hyperlipidemia, liver steatosis and oxidative stress in obese rats. The effects were more pronounced with encapsulation. Coffee parchment extract protected against fructose-induced obesity metabolic alterations; a better amelioration was observed with microcapsules which will increase the value of this coffee by-product.

Monoamine oxidase is a source of cardiac oxidative stress in obese rats: the beneficial role of metformin.

Diet-induced metabolic diseases, such as obesity, metabolic syndrome, and type 2 diabetes (T2DM) are the global threatening epidemics that share cardiovascular oxidative stress as common denominator. Monoamine oxidase (MAO) has recently emerged as a constant source of reactive oxygen species (ROS) in DM. Metformin, the first-line drug in T2DM, elicits cardiovascular protection via pleiotropic effects. The present study was aimed to assess the contribution of MAO to the early cardiac oxidative stress in a rat model of high-calorie junk food (HCJF) diet-induced obesity and prediabetes and whether metformin can alleviate it. After 6months of HCJF, rats developed obesity and hyperglycemia. Hearts were isolated and used for the evaluation of MAO expression and ROS production. Experiments were performed in the presence vs absence of metformin (10µM) and MAO-A and B inhibitors (clorgyline and selegiline, 10µM), respectively. Both MAO isoforms were overexpressed and led to increased ROS generation in cardiac samples harvested from the obese animals. Acute treatment with metformin and MAO inhibitors was able to mitigate oxidative stress. More important, metformin downregulated MAO expression in the diseased samples. In conclusion, MAO contributes to oxidative stress in experimental obesity and can be targeted with metformin.

Effects of Green Apple (Golden Delicious) and Its Three Major Flavonols Consumption on Obesity, Lipids, and Oxidative Stress in Obese Rats.

Obesity is becoming increasingly common all over the world and global strategies are accordingly being developed to prevent it. In order to support the strategies, the effects of green apple (Golden Delicious) and the consumption of its three major flavonols (quercetin-3-glucoside, quercetin-3-D-galactoside, and quercetin-3-rhamnoside) on body weight; the weight of liver, kidney, and spleen; some lipid parameters in serum; and total lipid ratios of liver and kidney and oxidative stress parameters of obese rats were studied. This study was conducted on two experimental groups: one of which was given an apple, and the other was given flavonols, in addition to their high-energy diet; along with a sham and a control rat group, for 4 weeks. According to results, there was no difference in body and organ weights between groups. The liver and kidney weights increased in obese rats, but there was no difference between the total lipid ratios in these organs. The addition of green apple and selected flavonols to the high-energy diet of rats was not sufficient to prevent the increase in body and organ weights, but it supported the reduction in some lipid fractions and in oxidative stress parameters of obese rats. Moreover, this study supported the argument that obesity causes most of the lipid fractions increase in serum and induces oxidative stress.

Anthocyanin-rich fraction from black rice, Oryza sativa L. var. indica "Luem Pua," bran extract attenuates kidney injury induced by high-fat diet involving oxidative stress and apoptosis in obese rats.

Obesity is acknowledged as being a world health problem and increases the risk of several chronic diseases including chronic kidney disease. High-fat diet consumption and obesity-related renal disease show a close correlation with increased oxidative stress. Black rice bran extract, (BRE) Oryza sativa L. variety "Luem Pua" contains a high anthocyanin content. This study evaluated the effects of an anthocyanin-rich fraction from BRE on renal function and oxidative stress in obese rats. Male Wistar rats were fed a normal diet (ND) or high-fat diet (HF) for 16 weeks. After this, the rats were given either vehicle (HF), BRE 100 (HF100) or BRE 200 mg/kg/day (HF200) orally for 8 weeks. The HF rats had increased body weight, visceral fat weight, plasma glucose, cholesterol and triglycerides. These parameters were normalized following HF100 administration and showed a decreasing trend with HF200. Serum creatinine and renal cortical MDA were increased in the HF group but these effects were attenuated by BRE. Negative kidney injury and histopathology changes were observed following a HF, but treatment with BRE reversed these deleterious effects. These results suggest that BRE could be used as a food supplement to improve metabolic disturbance and prevent kidney dysfunction in cases of obesity.

Timosaponin alleviates oxidative stress in rats with high fat diet-induced obesity via activating Nrf2/HO-1 and inhibiting the NF-κB pathway

Anemarrhena asphodeloides originated from the rhizome of Liliaceae Anemarrhena asphodeloides. One of the active pharmacological components of Anemarrhena asphodeloides is timosaponin (TSA), which reduces blood lipids and shows antioxidation and anti-inflammatory effects, but its mechanism is unclear. The objective of this study was to investigate the effect of TSA on oxidative stress induced by a long-term high-fat diet in obese rats. Body weight and the obesity index of the rats were measured during the experiment. Total antioxidant capacity (T-AOC), malondialdehyde (MDA), and glutathione peroxidase (GSH-Px) were used to detect oxidative stress indexes in serum and liver tissue. To observe the effect of TSA on the liver and adipose tissue of rats with oxidative stress, hematoxylin & eosin (H&E) staining was used. The p–NF–κB, NAD(P)H: quinone oxidoreductase 1 (NQO-1), Heme oxygenase 1 (HO-1), and Nrf2 in Nrf2/HO-1 and NF-κB pathways were assayed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. TSA was found to improve oxidative stress in obese rats by reducing MDA levels and increasing T-AOC and GSH-Px levels. Histological examination revealed that TSA effectively attenuated liver damage and improved obesity in rats. TSA was found to down-regulate the protein level of p–NF–κB and up-regulate the protein level of Nrf2/HO-1. These results suggested that TSA could effectively block inflammation and dyslipidemia in obese rats, thus improving oxidative stress, and its mechanism could be related to the Nrf2/HO-1 and NF-κB pathways.

The phytochemical epigallocatechin gallate prolongs the lifespan by improving lipid metabolism, reducing inflammation and oxidative stress in high-fat diet-fed obese rats.

We have recently reported that epigallocatechin gallate (EGCG) could extend lifespan in healthy rats. This study aimed to investigate the effects and mechanisms of a high dose of EGCG in extending the lifespan of obese rats. Ninety adult male Wistar rats were randomly divided into the control (NC), high‐fat (HF) and EGCG groups. Serum glucose and lipids, inflammation and oxidative stress were dynamically determined from adulthood to death, and the transcriptome and proteome of the liver were also examined. The median lifespans of the NC, HF and EGCG groups were 693, 599 and 683 days, respectively, and EGCG delayed death by 84 days in obese rats. EGCG improved serum glucose and lipids and reduced inflammation and oxidative stress associated with aging in obese rats induced by a high‐fat diet. EGCG also significantly decreased the levels of total free fatty acids (FFAs), SFAs and the n‐6/n‐3 ratio but significantly increased the n‐3 FFAs related to longevity. The joint study of the transcriptome and proteome in liver found that EGCG exerted its effects mainly by regulating the suppression of hydrogen peroxide and oxygen species metabolism, suppression of oxidative stress, activation of fatty acid transport and oxidation and cholesterol metabolism. EGCG significantly increased the protein expression of FOXO1, Sirt1, CAT, FABP1, GSTA2, ACSL1 and CPT2 but significantly decreased NF‐κB, ACC1 and FAS protein levels in the livers of rats. All the results indicate that EGCG extends lifespan by improving FFA metabolism and reducing the levels of inflammatory and oxidative stress in obese rats.

High-fat diet-induced metabolic syndrome and oxidative stress in obese rats are ameliorated by yogurt supplementation

The main objective of this experiment was to determine the effects of yogurt supplementation on fat deposition, oxidative stress, inflammation and fibrosis in the liver of rats with high-fat (HF) diet-induced obesity. Male Wistar rats were used in this study and were separated into the following four different groups: the control, control + yogurt, high fat and high fat+ yogurt groups. The high fat groups received a HF diet for eight weeks. A 5% yogurt (w/w) supplement was also provided to rats fed the HF diet. Yogurt supplementation prevented glucose intolerance and normalized liver-specific enzyme activities in the HF diet-fed rats. Yogurt supplementation also significantly reduced the levels of oxidative stress markers in the plasma and liver of HF diet-fed rats. Moreover, inflammatory cell infiltration, collagen deposition and fibrosis in the liver of HF diet-fed rats were also prevented by yogurt supplementation. Furthermore, yogurt supplementation normalized the intestinal lining and brush border in HF diet-fed rats. This study suggests that yogurt supplementation potentially represents an alternative therapy for the prevention of metabolic syndrome in HF diet-fed rats.

Extruded sorghum (Sorghum bicolor L.) improves gut microbiota, reduces inflammation, and oxidative stress in obese rats fed a high-fat diet

The aim of this study was to investigate the effects of extruded sorghum flour (ESF) on rats fed with a high-fat diet (HFD) on gut microbiota modulation, inflammation, and oxidative stress. Male Wistar rats were fed a normal diet (AIN-93 M, n = 8), HFD (n = 8), or HFD plus ESF replacing 50% cellulose and 100% corn starch (HFDS50, n = 8) or HFD plus ESF replacing 100% cellulose and 100% corn starch (HFDS100, n = 8) for eight weeks. ESF improved the composition of intestinal microbiota by increasing the proportion of the Bacteroidetes phylum instead of the Firmicutes phylum. Furthermore, ESF reduced the concentrations of p65 NF-κB in liver, seric resistin, lipids peroxidation and increase the total antioxidant capacity of plasma, the expression of superoxide dismutase, and the heat shock protein 72. In conclusion, ESF improves the intestinal dysbiosis, inflammation and oxidative stress in obese rats fed a hyperlipid diet.

G‐Hesperidin Supplementation Impairs the Beneficial Effects of Physical Exercise on the Body Composition, Biochemistry Profile and Oxidative Stress in Obese Rats

Obesity is a worldwide public health problem and its treatment includes limited dietary intake of saturated fats and physical activity. Obesity may be accompanied by metabolic changes and may cause several organic dysfunctions such as vascular dysfunctions due to reduced bioavailability of vasodilatory substances such as nitric oxide (NO). There are evidences that the reduced vasodilatory substances are related to increased reactive oxygen species (ROS), which leads to an oxidative stress. Additionally, the intake of antioxidant flavonoids has been largely proposed as a therapy for metabolic and cardiovascular disorders. Therefore, the aim of this work was to evaluate the effects of G‐ hesperidin supplementation (an antioxidant flavonoid) associated (or not) with physical exercise, on the body composition, lipidic metabolism, oxidative status and vascular function of obese rats. Obesity was induced by a hyperlipidic diet plus fructose given to 4 weeks‐old male Wistar rats, lasting 12 weeks. Physical training and/or antioxidant treatment started along with the 8th week of life and lasted 8 weeks further. It was evaluated the body compositon, lipid profile, oxidative status and mesenteric artery was removed for functional evaluation. After 12 weeks of hyperlipidic diet, rats presented higher body weight gain and body fat accumulation when compared to rats fed with standard chow. Treatment with G‐hesperidin did not change body weight gain and fat depot. Only physical training was able to reduce the body weight gain and fat accumulation. Furthermore, physical training modulated the oxidative status by increasing SOD activity, total antioxidant capacity and reducing lipid peroxidation. Treatment with G‐hesperidin did not affect oxidative status and when associated to physical training, decreased changes elicited by physical training. Hyperlipidic diet caused endothelial dysfunction, since the potency of acetylcholine was reduced in all groups fed with hyperlipidic diet. Treatment with G‐hesperidin and physical exercise did not alter the potency of acetylcholine. Potency of sodium nitroprusside was not changed by hyperlipidic diet whereas it was potentiated by physical training. Our results show that, in experimental model of obesity, physical exercise is able to modify body composition and biochemical parameters and improve general oxidative status of rats fed with hyperlipidic diet. Treatment with antioxidant flavonoid G‐hesperidin inhibited the benefit promoted by physical exercise.Support or Funding InformationFAPESP ‐ Fundação de Amparo à Pesquisa do Estado de São Paulo.

A cafeteria diet triggers intestinal inflammation and oxidative stress in obese rats

The gastrointestinal alterations associated with the consumption of an obesogenic diet, such as inflammation, permeability impairment and oxidative stress, have been poorly explored in both diet-induced obesity (DIO) and genetic obesity. The aim of the present study was to examine the impact of an obesogenic diet on the gut health status of DIO rats in comparison with the Zucker (fa/fa) rat leptin receptor-deficient model of genetic obesity over time. For this purpose, female Wistar rats (n 48) were administered a standard or a cafeteria diet (CAF diet) for 12, 14·5 or 17 weeks and were compared with fa/fa Zucker rats fed a standard diet for 10 weeks. Morphometric variables, plasma biochemical parameters, myeloperoxidase (MPO) activity and reactive oxygen species (ROS) levels in the ileum were assessed, as well as the expressions of proinflammatory genes (TNF-α and inducible nitric oxide synthase (iNOS)) and intestinal permeability genes (zonula occludens-1, claudin-1 and occludin). Both the nutritional model and the genetic obesity model showed increased body weight and metabolic alterations at the final time point. An increase in intestinal ROS production and MPO activity was observed in the gastrointestinal tracts of rats fed a CAF diet but not in the genetic obesity model. TNF-α was overexpressed in the ileum of both CAF diet and fa/fa groups, and ileal inflammation was associated with the degree of obesity and metabolic alterations. Interestingly, the 17-week CAF group and the fa/fa rats exhibited alterations in the expressions of permeability genes. Relevantly, in the hyperlipidic refined sugar diet model of obesity, the responses to chronic energy overload led to time-dependent increases in gut inflammation and oxidative stress.

비만 흰쥐에서 발효 서목태의 항산화 효과

This study was to examine the antioxidative activity of fermented Rhynchosia nulubilis (FRN) in obese rats. Oxidative stress due to reactive oxygen species (ROS) can cause oxidative damage to cells. Mitochondria are especially important in the oxidative stress as ROS have been found to be constantly generated as an endogen threat. Mitochondrial defense depends mainly on superoxide dismutase whereas microsomal defense depends on cat- alase, which is an enzyme abundant in microsomes. Seven weeks-aged female Sprague-Dawley rats were divided into four groups and fed high fat diets for 44 days. Also fermented Rhynchosia nulubilis was administered orally for 44 days at 7.5 ml/kg of body weight of rats. The antioxidative activities of fermented Rhynchosia nulubilis were mea- sured by the superoxide dismutase, catalase, malondialdehyde levels in liver homogenate. The levels of malondialde- hyde in FRN-treated groups were lower than those in obese groups. Superoxide dismutase and catalase levels were significantly increased. These results demonstrated that fermented Rhynchosia nulubilis had the inhibitive effects of oxidative stress in obese rats, suggesting that fermented Rhynchosia nulubilis would be used as an ingredient of the useful functional products.

Oxidative stress causes imbalance of renal renin angiotensin system (RAS) components and hypertension in obese Zucker rats.

BackgroundOxidative stress plays an important role in the pathogenesis of hypertension, especially in obesity‐related hypertension. The natriuretic and antinatriuretic components of the renal renin angiotensin system (RAS) maintain sodium homeostasis and blood pressure. Here, we test the hypothesis that increased oxidative stress leads to the imbalance of RAS components and hypertension in obese Zucker rats.Methods and ResultsLean and obese rats received vehicle or tempol, a superoxide dismutase mimetic in the drinking water for 4 weeks. Compared with vehicle‐treated lean rats, vehicle‐treated obese rats exhibited higher blood pressure and increased renal oxidative stress, accompanied by increased diuretic and natriuretic responses to AT1R antagonist (Candesartan) and AT2R agonist (CGP‐42112A) and reduced diuretic and natriuretic response to MasR agonist (Ang‐[1 to 7]). Moreover, obese rats had higher ACE, AT1R and AT2R, lower ACE2 and MasR expressions in the kidney. All of the above‐mentioned abnormalities were reversed to some degree by tempol treatment. In primary cultures of renal proximal tubular (RPT) cells from lean and obese rats, tempol treatment also increased AT2R, ACE2, and MasR expressions but decreased AT1R and ACE expressions in obese rats.ConclusionsTaken together, our study indicated that the imbalance of renal RAS components was associated with increased oxidative stress in obese rats. Furthermore, antioxidant treatment with tempol reversed the imbalance of renal RAS components and led to diuresis and natriuresis, which, at least in part, explains the blood pressure‐lowering effect of antioxidant supplementation in obesity‐related hypertension.

Liuwei Dihuang, a traditional Chinese herbal formula, suppresses chronic inflammation and oxidative stress in obese rats

To investigate the anti-inflammatory, anti-oxidative stress, and adipokine-ameliorating effects of Liuwei Dihuang (LWDH), a traditional Chinese herbal formula, in obese rats. After 2 weeks of acclimation with free access to regular rodent chow and water, obese-prone-caesarean-derived (OP-CD) rats were fed a modified AIN-93G diet containing 60% energy from fat. Treatment was performed twice daily by gavage feeding with 500, 1 500, or 3 500 mg/kg body weight LWDH suspended in water (n=12 rats per group). Twelve obese-resistant-CD (OR-CD) rats were fed the atherogenic diet and gavaged with water, and served as the normal control. Blood biomarkers of inflammation, oxidative stress and adiponectin were measured post-sacrifice and used to determine the treatment effect of LWDH and assess the suitability of OR/OP-CD rats for studying these parameters. After 9 weeks of treatment, LWDH lowered serum C-reactive protein (CRP) and tumour necrosis factor-α (TNF-α) levels. Serum interleukin-6 (IL-6) levels showed a tendency towards reduction, but were not significantly different from the OP-CD control. Liver superoxide dismutase (SOD) activity was increased in response to all three doses of LWDH, while the levels of reduced (GSH) and oxidized glutathione (GSSG) and thiobarbituric acid reactive substances (TBARS) were unchanged. Serum adiponectin levels were increased in response to oral administration of LWDH at the dose of either 500 or 1 500 mg/kg body weight. In addition, comparisons between OR-CD and OP-CD rats revealed differential, and for some biomarkers, conflicting characteristics of high-fat diet-fed OP-CD rats in reference to obese human subjects in terms of inflammatory and oxidative stress biomarkers and circulating adiponectin levels. The results show, for the first time, the anti-inflammatory, anti-oxidative stress and adiponectin-ameliorating effects of LWDH in obese rats. The suitability of the OR/OP-CD rat model as a research tool to study inflammation, oxidative stress, and adipokine production requires further investigation.

High-fat, low-carbohydrate diet alters myocardial oxidative stress and impairs recovery of cardiac function after ischemia and reperfusion in obese rats

Obesity is associated with elevated risk of heart disease. A solid understanding of the safety and potential adverse effects of high-fat, low-carbohydrate diet (HFLCD) similar to that used by humans for weight loss on the heart is crucial. High fat intake is known to promote increases in reactive oxygen species and mitochondrial damage. We hypothesized that there would be adverse effects of HFLCD on myocardial ischemia/reperfusion injury through enhancing oxidative stress injury and impairing mitochondrial biogenesis in a nongenetic, diet-induced rat model of obesity. To test the hypothesis, 250-g male Sprague-Dawley rats were fed an obesity-promoting diet for 7 weeks to induce obesity, then switched to HFLCD or a low-fat control diet for 2 weeks. Isolated hearts underwent global low flow ischemia for 60 minutes and reperfusion for 60 minutes. High-fat, low-carbohydrate diet resulted in greater weight gain and lower myocardial glycogen, plasma adiponectin, and insulin. Myocardial antioxidant gene transcript and protein expression of superoxide dismutase and catalase were reduced in HFLCD, along with increased oxidative gene NADPH oxidase-4 transcript and xanthine oxidase activity, and a 37% increase in nitrated protein (nitrotyrosine) in HFLCD hearts. The cardiac expression of key mitochondrial regulatory factors such as nuclear respiratory factor-1 and transcription factor A–mitochondrial were inhibited and myocardial mitochondrial DNA copy number decreased. The cardiac expression of adiponectin and its receptors was down-regulated in HFLCD. High-fat, low-carbohydrate diet impaired recovery of left ventricular rate-pressure product after ischemia/reperfusion and led to 3.5-fold increased injury as measured by lactate dehydrogenase release. In conclusion, HFLCD leads to increased ischemic myocardial injury and impaired recovery of function after reperfusion and was associated with attenuation of mitochondrial biogenesis and enhanced oxidative stress in obese rats. These findings may have important implications for diet selection in obese patients with ischemic heart disease.

Effects of exercise training on gingival oxidative stress in obese rats

ObjectiveThe purpose of the present study was to investigate the effects of exercise training on serum reactive oxygen species (ROS) level and gingival oxidative stress in obese rats fed a high-fat diet. DesignRats were divided into three groups (n=14/group): one control group (fed a regular diet) and two experimental groups (fed a high-fat diet with and without exercise training [treadmill: 5 days/week]). The rats were sacrificed at 4 or 8 weeks. The level of serum reactive oxidative metabolites (ROM) was measured as an indicator of circulating ROS. The level of 8-hydroxydeoxyguanosine (8-OHdG) and reduced-form glutathione (GSH)/oxidised-form glutathione (GSSG) ratio were determined to evaluate gingival oxidative stress. ResultsThe obese rats fed a high-fat diet without exercise training showed higher serum ROM levels [Carratelli Units (CARR U)] (mean±SD; 413±64) than the control (333±12) at 4 weeks (p=0.023). Such a condition resulted in higher 8-OHdG levels (ng/mg mtDNA) (0.97±0.18) (p<0.05) and a lower GSH/GSSG ratio (17.0±3.1) (p<0.05) in gingival tissues, compared to the control (0.55±0.13 for 8-OHdG and 23.6±5.8 for GSH/GSSG ratio) at 8 weeks. In addition, the obese rats fed a high-fat diet with exercise training showed lower serum ROM (623±103) (p<0.001) and gingival 8-OHdG levels (0.69±0.17) (p=0.012) than those without exercise training (1105±95 for ROM and 0.55±0.13 for 8-OHdG) at 8 weeks. ConclusionsObesity prevention by exercise training may effectively suppress gingival oxidative stress by decreasing serum ROS in rats.