Physical and psychological stress along with candle fumes induced-cardiopulmonary injury mimicking restaurant kitchen workers.

Restaurant kitchens are work areas where involve strict and hierarchal environments that promote opportunity for bullying and workplace aggression and violence. These physical and psychological stress and fumes ultimately trigger severe occupational stress by disrupting the body's homeostasis that might induce cardiopulmonary injury. The study aimed to investigate the physical and psychological stress and candle fumes on cardiopulmonary injury in an animal model mimicking a restaurant kitchen worker. Social disruption stress (SDR) mice were exposed to scented candle fumes (4.5 h/d, 5 d/wk) in an exposure chamber for 8 weeks. Exposure to burning scented candles failed to reduce serum corticosterone level and increased proinflammatory cytokines levels and NF-ƙB activity in the lung. In addition, burning scented candle fumes synergistically increased SDR-induced serum LDH, CPK, CKMB levels, proinflammatory cytokines production as well as NF-ƙB activation in the lung and heart. Further, cardiac HIF-1α and BNP levels were also increased. We conclude that the physical and psychological stress along with candle fumes might induce cardiopulmonary injury in mice. These results could be extrapolated to restaurant kitchen workers.

Dietary Ziziphus jujuba Fruit Attenuates Colitis-Associated Tumorigenesis: A Pivotal Role of the NF-κB/IL-6/JAK1/STAT3 Pathway.

Inflammatory bowel disease (IBD) including ulcerative colitis (UC) is one of the risk factors for the development of colitis-associated colon cancer (CAC). CAC is a type of colorectal cancer (CRC), the third leading cause of cancer death. Ziziphus jujuba (ZJ) fruit contains bioactive components such as polysaccharides, triterpenoid acid, and flavonoids, and it has shown anti-inflammatory property. The aim of the study was to investigate the protective effect of dietary ZJ on colitis-associated colorectal tumorigenesis in mice. Mice (n = 42, two sets) were injected with azoxymethane (AOM) followed by three cycles of 2% (w/v) dextran sulfate sodium (DSS) in drinking water to induce CAC. Simultaneously, those mice were fed with ZJ diet for 70 days (5% or 10% w/w). Data were analyzed by ANOVA followed by LSD Bonferroni test. Dietary ZJ decreased fecal blood, diarrhea, disease activity index (DAI), spleen weight (P < 0.001), and the number of tumors (P < 0.001). In addition, dietary ZJ increased colon length (P < 0.001) and suppressed the activation of NF-кB/IL-6/JAK1/STAT3 signaling pathway. In conclusion, we suggest that dietary ZJ attenuates inflammation by interfering NF-κB/IL-6/JAK1/STAT3 signaling pathway, thereby inhibits AOM/DSS-induced colon tumorigenesis in mice.

Daily sesame oil supplementation mitigates ketoconazole-induced oxidative stress-mediated apoptosis and hepatic injury.

Ketoconazole (KCZ) is the most commonly used systemic antifungal drug. However, long-term treatment of KCZ induces hepatic injury. Oxidative stress is involved in KCZ-induced hepatic injury. Oxidative stress plays an important role in apoptosis-associated hepatic damage. Sesame oil is rich in potent antioxidants and antifungal constituents. It attenuates hepatic injury by inhibiting oxidative stress. Thus, sesame oil may protect against KCZ-induced oxidative stress, apoptosis and hepatic damage. The aim of the present study was to investigate the protective effect of sesame oil as a nutritional supplement on KCZ-induced hepatic injury in mice. KCZ (300 mg/kg/day) was administered by gastric intubation; 30 min later, sesame oil (0, 0.0625, 0.125, 0.25 or 0.5 ml/kg/day; p.o.) was administered to mice for 14 days. Blood and liver tissue were collected. Hepatic injury was evaluated by serum biochemistry and histology. Oxidative stress was evaluated by myeloperoxidase activity, p47-phox, reactive oxygen species generation, lipid peroxidation and glutathione level. Apoptosis was evaluated by p53, caspase-3, Bcl-2, Bax and Cyto-C expression. Osteopontin was measured to assess liver healing. Sesame oil attenuated hepatic injury; it also decreased oxidative stress and apoptosis in KCZ-treated mice. Sesame oil may be used as a nutritional supplement with existing antifungal therapies to neutralize the adverse hepatotoxic nature of antifungal drugs by attenuating hepatic apoptosis through redox system to protect and heal liver injury in KCZ-treated mice.

Dietary Ziziphus jujuba Fruit Influence on Aberrant Crypt Formation and Blood Cells in Colitis-Associated Colorectal Cancer in Mice.

Ziziphus jujuba (ZJ) fruit is rich in bioactive functional components such as polysaccharides, triterpenoid acid, flavonoids and oleamide. It has been commonly used in the treatment of various diseases including diabetes, digestive disorders, diarrhea, skin infections, liver and urinary complaints. However, dietary effects with regard to chemoprevention of colon cancer have not been studied. The present study was performed to evaluate the protective effects of dietary ZJ against colitis-associated colon carcinogenesis in azoxymethane (AOM)-dextran sodium sulphate (DSS)-treated mice. AOM was injected (10 mg/kg b.wt., i.p.) and three cycles of 2% DSS in drinking water for 7 days with 14 days of normal drinking water in-between were administered to induce colitis-associated colon cancer. ZJ fruit was supplemented into feed at levels of 5 and 10%. Dietary ZJ significantly attenuated aberrant crypt foci (ACF) formation and also decreased the progression of hyperplasia to dysplasia. In addition, it significantly reduced circulating white blood cells, lymphocytes, neutrophils, monocytes, eosinophils, basophils and platelets compared to colon cancer mice. We conclude that ZJ supplementation may delay the progression of colon cancer from hyperplasia to dysplasia and ultimately adenocarcinoma and cancer. In addition, it decreased circulating tumor-related leukocytes, main regulators of cancer inflammation. Dietary consumption of ZJ fruit attenuated the formation of ACF and delayed the progression of colon cancer.

Curative effect of sesame oil in a rat model of chronic kidney disease.

AIM: Chronic kidney disease causes a progressive and irreversible loss of renal function. We investigated the curative effect of sesame oil, a natural, nutrient-rich, potent antioxidant, in a rat model of chronic kidney disease. METHODS: Chronic kidney disease was induced by subcutaneously injecting uni-nephrectomized rats with deoxycorticosterone acetate (DOCA) and 1% NaCl [DOCA/salt] in drinking water. Four weeks later, the rats were gavaged with sesame oil (0.5 or 1 mL/kg per day) for 7 days. Renal injury, histopathological changes, hydroxyl radical, peroxynitrite, lipid peroxidation, Nrf2, osteopontin expression, and collagen were assessed 24 h after the last dose of sesame oil. RESULTS: Blood urea nitrogen, creatinine, urine volume, and albuminuria were significantly higher in the DOCA/salt treated rats than in control rats. Sesame oil significantly decreased these four tested parameters in DOCA/salt treated rats. In addition, creatinine clearance rate and nuclear Nrf2 expression were significantly decreased in the DOCA/salt treated rats compared to control rats. Sesame oil significantly decreased hydroxyl radical, peroxynitrite level, lipid peroxidation, osteopontin, and renal collagen deposition, but increased creatinine clearance rate and nuclear Nrf2 expression in DOCA/salt treated rats. CONCLUSION: We conclude that supplementation of sesame oil mitigates DOCA/salt induced chronic kidney disease in rats by activating Nrf2 and attenuating osteopontin expression and inhibiting renal fibrosis in rats.

Sesame oil mitigates nutritional steatohepatitis via attenuation of oxidative stress and inflammation: a tale of two-hit hypothesis.

Nonalcoholic fatty liver disease, the most common chronic liver disorder worldwide, comprises conditions from steatosis to nonalcoholic steatohepatitis (NASH) and cirrhosis. NASH is associated with an increased risk of hepatocellular carcinoma. Sesame oil, a healthful food, increases resistance to oxidative stress, inflammation and protects against multiple organ injury in various animal models. We investigated the protective effect of sesame oil against nutritional steatohepatitis in mice. C57BL/6 J mice were fed with methionine-choline deficient (MCD) diet for 28 days to induce NASH. Sesame oil (1 and 2 ml/kg) was treated from 22nd to 28th day. Body weight, steatosis, triglycerides, aspartate transaminase, alanine transaminase, nitric oxide, malondialdehyde, tumor necrosis factor-α, interlukin-6, interleukin-1ß, leptin, and transforming growth factor-ß1 (TGF-ß1) were assessed after 28 days. All tested parameters were higher in MCD-fed mice than in normal control mice. Mice fed with MCD diet for 4 weeks showed severe liver injury with steatosis, oxidative stress, and necrotic inflammation. In sesame-oil-treated mice, all tested parameters were significantly attenuated compared with MCD-alone mice. Sesame oil inhibited oxidative stress, inflammatory cytokines, leptin, and TGF-ß1 in MCD-fed mice. In addition, histological analysis showed that sesame oil provided significant protection against fibrotic collagen. We conclude that sesame oil protects against steatohepatitic fibrosis by decreasing oxidative stress, inflammatory cytokines, leptin and TGF-ß1.

Therapeutic oral sesame oil is ineffectual against monocrotaline-induced sinusoidal obstruction syndrome in rats.

BACKGROUND: The chemotherapeutic drug oxaliplatin causes sinusoidal obstruction syndrome (SOS), which is analogous to that of monocrotaline-induced SOS. Sesame oil is a nutrient-rich antioxidant in alternative medicine. It contains phenol, sesamin, sesamol, and sesamolin, all of which contribute to its antioxidant property. The authors investigated the therapeutic effect of oral sesame oil against monocrotaline-induced SOS in rats. METHODS: Male Sprague-Dawley rats were gavaged with monocrotaline (90 mg/kg) to induce SOS. Control rats were treated with saline only at 0 and 24 hours. Sesame oil (0.5, 1, 2, or 4 mL/kg, orally) was given 24 hours after monocrotaline in rats. Blood samples were collected at 24 and 48 hours after monocrotaline was given to assess the level of aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Histopathology was also assessed 48 hours after monocrotaline was given. RESULTS: AST and ALT were significantly higher in monocrotaline-treated rats than in control rats. Oral sesame oil did not decrease AST and ALT in monocrotaline-treated rats. In addition, liver pathology revealed that oral sesame oil had no therapeutic effect against SOS. CONCLUSION: Oral sesame oil is therapeutically ineffectual against monocrotaline-induced SOS.

Prophylactic and therapeutic effects of a subcutaneous injection of sesame oil against iron-induced acute renal injury in mice.

BACKGROUND: Iron intoxication causes acute nephrotoxicity in animals and humans. Sesame oil, a healthful food, increases resistance to lipid peroxidation and protects against multiple organ injury in various animal models. The authors examined the prophylactic and therapeutic effects of a subcutaneous injection of sesame oil against iron-induced acute renal injury in mice. METHODS: Iron intoxication in mice was induced with an intraperitoneal injection (2 mg/kg) of ferric-nitrilotriacetate (Fe-NTA). Various doses of sesame oil (0, 1, 2, and 4 mL/kg, subcutaneously) were given immediately after (prophylactic) or 30 minutes after (therapeutic) the Fe-NTA injection. Renal injury was assessed by the rise in serum blood urea nitrogen (BUN) and creatinine (CRE) levels 3 hours after the Fe-NTA injection. RESULTS: One hour after the Fe-NTA injection, serum BUN and CRE levels were significantly higher in Fe-NTA-treated mice than in saline-treated controls; 3 and 6 hours after the Fe-NTA injection, they were dose-dependently and significantly lower in all sesame oil-treated groups than in the group treated only with Fe-NTA and saline. CONCLUSION: A subcutaneous injection of sesame oil had both prophylactic and therapeutic effects against iron-induced acute renal injury in mice.

Anti-hepatotoxic effects of 3,4-methylenedioxyphenol and N-acetylcysteine in acutely acetaminophen-overdosed mice.

3,4-Methylenedioxyphenol (sesamol) is effective against acetaminophen-induced liver injury in rats. Whether sesamol's anti-hepatotoxic effect is comparable to that of N-acetylcysteine has never been studied. We investigated the anti-hepatotoxic effects of sesamol and N-acetylcysteine on acetaminophen-induced hepatotoxicity in mice. Equimolar doses (1 mmol/kg) of sesamol and N-acetylcysteine significantly inhibited acetaminophen (300 mg/kg)-increased serum aspartate transaminase and alanine transaminase levels 6 h post-administration. Sesamol and N-acetylcysteine maintained hepatic glutathione levels and inhibited lipid peroxidation. Moreover, the combination of sesamol and N-acetylcysteine antagonistically inhibited sesamol's protection against acetaminophen-induced liver injury. We conclude that the protective effect of sesamol against acetaminophen-induced liver damage is comparable to that of N-acetylcysteine by maintaining glutathione levels and inhibiting lipid peroxidation in mice.

Effects of sesame oil against after the onset of acetaminophen-induced acute hepatic injury in rats.

BACKGROUND: Acetaminophen (APAP) is a safe and effective analgesic and antipyretic when used at therapeutic levels. However, an acute or cumulative overdose can cause severe liver injury with the potential to progress to liver failure in humans and experimental animals. Much attention has been paid to the development of an antioxidant that protects against APAP-induced acute hepatic injury. Hence, we aimed to investigate the effect of sesame oil against after the onset of acute hepatic injury in APAP-overdosed rats. METHODS: Male Wistar rats were first given 2 oral doses (1,000 mg/kg each) of APAP (at 0 and 24 hours) and then 1 oral dose of sesame oil (8 mL/kg at 24 hours). RESULTS: After 48 hours, APAP increased aspartate and alanine aminotransferase levels in the rats' serum and centrilobular necrosis in liver tissue. In addition, APAP significantly decreased the rats' glutathione levels and mitochondrial aconitase activity, but increased superoxide anion, hydroxyl radical, and lipid peroxidation levels. Oral sesame oil (8 mL/kg, given at 24 hours) reversed all APAP-altered parameters and protected the rats against APAP-induced acute liver injury. CONCLUSION: We hypothesize that sesame oil acts as a useful agent that maintains intracellular glutathione levels and inhibits reactive oxygen species, thereby protecting rats against after the onset of APAP-induced acute oxidative liver injury.

Protective effect of sesamol on the pulmonary inflammatory response and lung injury in endotoxemic rats.

We investigated the effect of sesamol on systemic lipopolysaccharide (LPS)-induced lung inflammation in rats. Sesamol decreased lung edema and injury, significantly decreased LPS-induced cell counts, protein concentration, tumor necrosis factor (TNF)-alpha, and nitrite levels in bronchoalveolar lavage fluid, and decreased the TNF-alpha, nitrite, and inducible nitric oxide synthase protein expression in lung tissue. Further, sesamol significantly inhibited LPS-induced TNF-alpha, nitrite, inducible nitric oxide synthase expression, and nuclear factor-kappaB activation levels in primary alveolar macrophages. We hypothesize that sesamol attenuates systemic LPS-induced lung inflammation by inhibiting the alveolar macrophage inflammatory response in rats.

Sesame oil attenuates hepatic lipid peroxidation by inhibiting nitric oxide and superoxide anion generation in septic rats.

BACKGROUND: Sepsis is a major cause of mortality in the intensive care unit. Oxidative stress plays an important role in the pathogenesis of organ failure during sepsis. Sesame oil decreases circulating oxygen free radicals in septic rats; however, its effect on hepatic oxidative status is unknown. The authors examined the effect of sesame oil on hepatic lipid peroxidation in septic rats. METHODS: Hepatic injury was induced using cecal ligation and puncture (CLP). Rats were divided into 4 groups: sham, rats given a sham operation without CLP; SO, rats given sesame oil alone; CLP, rats given saline and then CLP; and CS, rats given sesame oil and then CLP. All rats were first given a 1-week daily oral supplement of sesame oil or saline (4 mL/kg/d) and then CLP or a sham operation. The authors assessed hepatic oxidative stress by determining hepatic lipid peroxidation, hydroxyl radical, superoxide anion, and nitric oxide levels 12 hours after CLP. They also assessed xanthine oxidase activity and nitric oxide synthase expression. RESULTS: Hepatic lipid peroxidation (P < .0001), hydroxyl radical (P < .05), superoxide anion (P < .05), and nitrite (P < .05) levels were significantly lower in sesame oil-treated septic rats. Furthermore, sesame oil significantly reduced xanthine oxidase activity (P < .01) and inducible nitric oxide synthase expression (P < .005) in septic rats. CONCLUSIONS: Sesame oil might attenuate hepatic lipid peroxidation by inhibiting superoxide anion and nitric oxide, at least partially, in experimental septic rats.

Sesame oil does not show accumulatively enhanced protection against oxidative stress-associated hepatic injury in septic rats.

BACKGROUND: Sepsis is one of the major causes of death reported in intensive care units. A daily supplement of sesame oil for 1 week significantly attenuates oxidative stress-associated hepatic injury in septic rats. However, the excess intake of sesame oil may be associated with a health risk. This study investigates the effect of accumulative sesame oil on oxidative stress-associated hepatic injury after cecal ligation and puncture in rats. METHODS: Sesame oil was administered daily (4 mL/kg/d, orally) to rats, and the total intake of sesame oil ranged from 0 (control) to 140 mL/kg before cecal ligation and puncture in 9 groups of rats. Oxidative stress was examined by determining the levels of lipid peroxidation and glutathione. Hepatic injury was evaluated by measuring serum levels of aspartate aminotransferase and alkaline phosphatase. RESULTS: Rats that received sesame oil for 4 and 5 weeks had a lower body weight gain compared with those that received saline. Lipid peroxidation was decreased in the 20-mL/kg and 28-mL/kg groups, but it was increased in the 140-mL/kg group compared with the control group. Glutathione levels were increased in the < or =28-mL/kg groups compared with the control group. Serum levels of aspartate aminotransferase and alkaline phosphatase were reduced in the < or =28-mL/kg groups compared with the control group. CONCLUSION: Sesame oil does not demonstrate accumulatively enhanced protection against oxidative stress-associated hepatic injury after cecal ligation and puncture in rats.

The effect of sesamol on systemic oxidative stress and hepatic dysfunction in acutely iron-intoxicated mice.

This study investigated the effect of sesamol (3,4-methylenedioxyphenol) on systemic oxidative stress and hepatic function in acutely iron-intoxicated mice. Sesamol reduced the levels of lipid peroxidation, hydroxyl radical, iron production and superoxide anion generation, and xanthine oxidase activity in iron-intoxicated mice. In addition, sesamol decreased the serum levels of aspartate aminotransferase and alanine aminotransferase, and ameliorated iron-intoxication-induced histological changes in the liver. In summary, sesamol might attenuate systemic oxidative stress by reducing xanthine oxidase and improving hepatic function in iron-intoxicated mice.

Sesame oil attenuates acute iron-induced lipid peroxidation-associated hepatic damage in mice.

Acute iron intoxication from the accidental ingestion of iron-containing preparations is one important cause of death in children. The aim of this study was to investigate the protective effect of sesame oil on acute iron-induced lipid peroxidation (LPO) and hepatic injury in mice. Acute iron intoxication was induced by giving ferric nitrilotriacetate to mice. Hepatic function was assessed using blood biochemistry. Free radicals were determined using a high-performance chemiluminescence analyzer. Ferric nitrilotriacetate increased serum ferrous (Fe) and LPO levels, and induced acute hepatic injury. Sesame oil (a) dose-dependently decreased acute iron-induced LPO and hepatic injury, (b) reduced acute iron-associated hydroxyl radical and superoxide anion generation, and (c) inhibited the activity of xanthine oxidase in acute iron intoxication. Thus, sesame oil might ameliorate LPO and acute hepatic injury by inhibiting xanthine oxidase-initiated superoxide anion generation, thereby reducing hydroxyl radical production, at least partially, in acutely iron-intoxicated mice.

Attenuation of endotoxin-induced oxidative stress and multiple organ injury by 3,4-Methylenedioxyphenol in rats.

Endotoxin is a potent inducer of lipid peroxidation (LPO), which is associated with the development of endotoxemia. 3,4-Methylenedioxyphenol (sesamol) is one of the sesame oil lignans with a high anti-LPO effect. Whether sesamol can attenuate endotoxin-induced LPO and multiple organ injury is unknown. After a dose response for sesamol in endotoxin-challenged rats was established, experiments were conducted to assess its effects on hydroxyl radical, peroxynitrite, and superoxide anion counts, activities of superoxide dismutase, catalase, and glutathione peroxidase, as well as the production of nitric oxide (NO) and the expression of inducible NO synthase. In addition, the effects of sesamol on endotoxin-induced hepatic and renal injuries were assessed. Sesamol (a) dose dependently reduced serum LPO inendotoxin-challenged rats, (b) decreased hydroxyl radical and peroxynitrite, but not superoxide anion counts, (c)increased the activities of superoxide dismutase, catalase, and glutathione peroxidase in endotoxin-treated rats, (d)reduced NO production and inducible NO synthase expression, and (e) attenuated hepatic and renal injuries induced by endotoxin in rats. We concluded that sesamol might protect against organ injury by decreasing NO-associated LPO in endotoxemic rats.

Effect of sesame oil on oxidative-stress-associated renal injury in endotoxemic rats: involvement of nitric oxide and proinflammatory cytokines.

This study aimed to investigate the effect of sesame oil on oxidative stress-associated renal injury induced by lipopolysaccharide in rats. The effects of sesame oil on renal injury, oxidative stress, hydroxyl radical, superoxide anion, nitric oxide, and proinflammatory cytokines were assessed after a lipopolysaccharide challenge. Sesame oil attenuated lipopolysaccharide-induced renal injury, decreased lipid peroxidation, increased the activities of superoxide dismutase, catalase, and glutathione peroxidase, reduced hydroxyl radical generation and nitric oxide production, and had no effect on superoxide anion generation in lipopolysaccharide-challenged rats. In addition, sesame oil significantly decreased tumor necrosis factor-alpha and interleukin 1beta production 1 and 6 h, respectively, after lipopolysaccharide administration in mice. Thus, sesame oil attenuates oxidative stress-associated renal injury via reduction of the production of nitric oxide and the generation of proinflammatory cytokines in endotoxemic rats.

Effects of sesame oil on oxidative stress and hepatic injury after cecal ligation and puncture in rats.

Oxidative stress is known to be involved in the development of organ failure and death in sepsis. Sesame oil attenuates oxidative stress induced by endotoxin; however, whether sesame oil is still effective in rats with sepsis has never been investigated. The aim of the present study was to determine the effect of sesame oil on oxidative stress-associated hepatic injury in cecal ligation and puncture-induced rats with sepsis. We examined the effect of sesame oil (4 mL/kg daily for 1 week) on lipid peroxidation, hydroxyl radical, superoxide anion, and nitrite levels in rats with sepsis. In addition, hepatic injury was also assessed by blood biochemistry. Sesame oil significantly decreased lipid peroxidation and serum nitrite levels, but affected neither superoxide anion nor hydroxyl radical in cecal ligation and puncture-treated rats. Furthermore, sesame oil significantly attenuated cecal ligation and puncture-induced hepatic injury in rats. Nevertheless, oxidative stress and hepatic injury were not affected by corn oil or mineral oil in rats with sepsis. Thus, attenuation of oxidative stress and hepatic injury may be associated with inhibition of nitric oxide in sesame oil-associated protection in rats with sepsis.

Parenteral sesame oil attenuates oxidative stress after endotoxin intoxication in rats.

Sesame oil is regarded as a daily nutritional supplement to increase cell resistance to lipid peroxidation. The aims of this study were to examine the effects of parenteral sesame oil on oxidative stress and hepatic disorder induced by lipopolysaccharide and to determine the defense mechanisms involved in sesame oil-associated anti-oxidative effects in rats. Oxidative stress was induced by lipopolysaccharide (5 mg/kg, intraperitoneally) and assessed by determination of lipid peroxidation. Sesame oil (8 ml/kg, subcutaneously) was given 3 h after lipopolysaccharide, and lipid peroxide levels, hydroxyl radical, superoxide anion, the enzyme activities of superoxide dismutase and catalase as well as the levels of glutathione and nitrite were examined 6 h after lipopolysaccharide. Hepatic function was assessed by determining the activities of serum aspartate aminotransferase and alkaline phosphatase. Sesame oil reduced lipid peroxidation and hydroxyl radical, but failed to affect superoxide anion. Superoxide dismutase and catalase were increased, but glutathione was not affected, and the levels of nitrite were reduced. Further, sesame oil-treated groups showed attenuated hepatic disorder in lipopolysaccharide-treated rats. Thus, parenteral sesame oil can be used to attenuate oxidative stress and relieve hepatic disorder after lipopolysaccharide intoxication in rats.