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Natural antioxidant compounds have different mechanisms of treatment and prevention against various diseases due to their richest ingredients. There are several antioxidants used today, such as phytogenic ingredients, flavonoids, capsaicin, spirulina, beta-glucan, polyphenol etc. Besides the outbreak of diseases, the ability to scavenge oxidative conditions of the natural antioxidants have been notably important. Thereby, therapeutic strategies of diseases have been interested by researchers. Try to seek a kind of effects of natural antioxidants to various diseases, especially viral or pandemic diseases are being important nowadays. This chapter we’ll mention about how to viral or pandemic disease’s effects on oxidative status in both animals and humans, and what kind of phytochemical ingredients would be a positive effect on. At the same time, the latest advances about these natural antioxidant compounds and pharmaceuticals will be critically highlighted and discussed with newest literatures.

Saccharomyces is a eukaryotic organism that possesses approximately 6,000 known genes since 1996. It has long been used for food, bakeries, drinks, and therapeutics due to its many ingredients and its role in several mechanisms. Saccharomyces can be used as an experimental organism for medicinal products in the pharmaceutical industry. Particularly in public health, the use of Saccharomyces in the production of vaccines is remarkable. It has been alleviated that this yeast helps clarify the function of individual proteins in pathogenic viruses. To clarify virus life and host interactions, virus replication systems in Saccharomyces were interested in scientists. The new antiviral strategies with yeasts suggest the biological mechanism of a pathogen virus. Due to the variety of diseases and current epidemic conditions, these organisms play an essential role in prevention and treatment. This chapter will try to update Saccharomyces’ scientific discoveries with the most recent and up-to-date literature.

Stress is a complex phenomenon and exposure to stress results in a series of reactions in the organism, including alterations in behaviour and various physiological changes. Role of nutrition in the maintenance of homeostatic mechanisms, including the stress, is very dense. The current study aimed to evaluate the potential effects of Spirulina (Arthrospira) platensis against mix stress models. For this purpose, 36 Sprague-Dawley male rats were allocated into four groups; 1. Control(C), 2. Stress(S), 3. S.platensis (Sp) and 4. S. platensis + Stress (SpS). S. platensis was applied to Sp and SpS groups by oral gavage (1500 mg/kg/day) for 28 days. All rats were exposed to light : dark cycle (long lightening period; 18h light : 6h dark) stress for 14 days. Also, S and SpS groups were stressed with additional mix stress by leaving in crowded environment and hosting alone under long lightening period. The animals which fed with S. platensis, shown significant changes in the numbers of circulating leukocytes, % of neutrophils, and the neutrophil : lymphocyte ratio. However, there were no significant differences in the morphological parameters. In conclusion, the possible preventive effect of S. platensis on hematological parameters was shown in a rat’s stress model of social stress which was included mix stress under long lightening period.

Setting exposure standards for environmental pollutants may consider the aged as a susceptible population but the few published studies assessing susceptibility of the aged to air pollutants are inconsistent. Episodic ozone (O-3) is more reflective of potential exposures occurring in human populations and could be more harmful to the aged. This study used radiotelemetry to monitor heart rate (HR), core temperature (T-c) and motor activity (MA) in adult (9-12 months) and senescent (20-24 months) male, Brown Norway rats exposed to episodic O-3 (6 h/day of 1 ppm O-3 for 2 consecutive days/week for 13 weeks). Acute O-3 initially led to marked drops in HR and T-c. As exposures progressed each week, there was diminution in the hypothermic and bradycardic effects of O-3. Senescent rats were less affected than adults. Acute responses were exacerbated on the second day of O-3 exposure with adults exhibiting greater sensitivity. During recovery following 2 d of O-3, adult and senescent rats exhibited an elevated Tc and HR during the day but not at night, an effect that persisted for at least 48 h after O-3 exposure. MA was elevated in adults but not senescent rats during recovery from O-3. Overall, acute effects of O-3, including reductions in HR and T-c, were attenuated in senescent rats. Autonomic responses during recovery, included an elevation in T-c with a pattern akin to that of a fever and rise in HR that were independent of age. An attenuated inflammatory response to O-3 in senescent rats may explain the relatively heightened physiological response to O-3 in younger rats.

Physical restraint of rodents is needed for nose-only exposure to airborne toxicants and is also used as a means of psychological stress. Hyperthermia is often observed in restrained rats, presumably as a result of impairments in heat dissipation. However, such a hyperthermic response should be dependent on the prevailing ambient conditions. To understand how ambient temperature (T(a)) affects the thermoregulatory response to restraint, core temperature (T(c)) and heart rate (HR) were monitored by telemetry in rats subjected to 1 h of physical restraint while T(a) was maintained at 14-30 °C in 2 °C increments. The T(c) of unrestrained rats was unaffected by T(a). During restraint, T(c) was elevated at ambient temperatures with the exception of 14 °C, at which the rats became mildly hypothermic. There was an inverse relationship between T(a) and HR in both unrestrained and restrained rats; however, HR was significantly elevated in restrained rats at all ambient temperatures except 22 and 24 °C. Heat loss from the tail, estimated from T(c) and tail skin temperature, was markedly reduced at all but the highest ambient temperatures in restrained rats. The data suggest that the T(a) limits of normothermia are narrowed in the restrained rat. That is, between 16 and 20 °C, the rat maintains a relatively stable T(c) that is slightly elevated above that of the unrestrained rat. At ambient temperatures above or below this range, the rat shows signs of hyperthermia and hypothermia, respectively. In contrast, the limits of normothermia for unrestrained rats range from 14 (or lower) to 30 °C. Overall, the ideal T(a) for restrained rats appears to be 20 °C and no higher than 22 °C for the thermoregulatory system to maintain a regulated T(c) in rats well adapted to physical restraint.

In this study, we evaluated the hypothesis that long term dietary restriction would have beneficial effects on the oxidative stress and antioxidant enzyme systems in liver, heart and kidney in adult mate rats undergoing different intensities of swimming exercise. Sixty male, Sprague-Dawley rats were assigned as either dietary restricted on every other week day (DR) or fed ad libitum (AL) groups, and each group was further subdivided into sedentary, endurance swimming exercise training (submaximal exercise) and exhaustive swimming exercise (maximal exercise) groups. Animals in the submaximal exercise group swam 5 days/week for 8 weeks, while maximal exercise was performed as an acute bout of exercise. In parallel with the increase in the intensity of the exercise, the degree of lipid peroxidation and protein oxidation were increased in both the DR and AL groups; however the rate of increase was lower in the DR group. Reduced glutathione (GSH), glutathione peroxidase (GSH-Px) and glutathione reductase (GR) enzyme activities were lower in the DR group than in the AL group. In parallel with the increase in exercise intensity, GSH and GR enzyme activities decreased, whereas an increase was observed in GSH-Px enzyme activity. In conclusion, the comparison between the DR and AL groups with the three swimming exercise conditions shows that the DR group is greatly protected against different swimming exercise-induced oxidative stress compared with the AL group.

The main goal of 2-stage liver transplant is to provide time to obtain a new liver source. We describe our experience of 3 patients with 3 different clinical conditions. A 57-year-old man was retransplanted successfully with this technique due to hepatic artery thrombosis. However, a 38-year-old woman with fulminant toxic hepatitis and a 5-year-old-boy with abdominal trauma had poor outcome. This technique could serve as a rescue therapy for liver transplant patients who have toxic liver syndrome or abdominal trauma. These patients required intensive support during long anhepatic states. The transplant team should decide early whether to use this technique before irreversible conditions develop.

Elevating ambient temperature above thermoneutrality exacerbates toxicity of most air pollutants, insecticides, and other toxic chemicals. On the other hand, safety and toxicity testing of toxicants and drugs is usually performed in mice and rats maintained at sub-thermoneutral temperatures of similar to 22 degrees C. When exposed to chemical toxicants under these relatively cool conditions, rodents typically undergo a regulated hypothermic response, characterized by preference for cooler ambient temperatures and controlled reduction in core temperature. Reducing core temperature delays the clearance of most toxicants from the body; however, a mild hypothermia also improves recovery and survival from the toxicant. Raising ambient temperature to thermoneutrality and above increases the rate of clearance of the toxicant but also exacerbates toxicity. Furthermore, heat stress combined with work or exercise is likely to worsen toxicity. Body temperature of large mammals, including humans, does not decrease as much in response to exposure to a toxicant. However, heat stress can nonetheless worsen toxic outcome in humans through a variety of mechanisms. For example, heat-induced sweating and elevation in skin blood flow accelerates uptake of some insecticides. Epidemiological studies suggest that thermal stress may exacerbate the toxicity of airborne pollutants such as ozone and particulate matter. Overall, translating results of studies in rodents to that of humans is a formidable task attributed in part to the interspecies differences in thermoregulatory response to the toxicants and to thermal stress. Published 2014.

Developmental exposure to endocrine disrupting drugs and environmental toxicants has been shown to alter a variety of physiological processes in mature offspring. Body (core) temperature (T-c) is a tightly regulated homeostatic system but is susceptible to disruptors of the hypothalamic pituitary thyroid (HPT) axis. We hypothesized that thermoregulation would be disrupted in adult offspring exposed perinatally to an HPT disruptor. Propylythiouracil (PTU) was used as a prototypical compound because of its well known antithyroidal properties. FLU was added to the drinking water of pregnant rats in concentrations of 0, 1, 2, 3, and 10 ppm from gestational day (GD) 6 through postnatal day (PND) 21. Adult male offspring were implanted with radiotransmitters to monitor T-c and motor activity (MA) and were observed undisturbed at an ambient temperature of 22 degrees C for 12 consecutive days. Data were averaged into a single 24 hour period to minimize impact of ultradian changes in T-c and MA. All treatment groups showed a distinct circadian temperature rhythm. Rats exposed to 10 ppm FLU exhibited a marked deviation in their regulated T-c with a reduction of approximately 0.4 degrees C below that of controls throughout the daytime period and a smaller reduction at night. Rats exposed to 1 or 2 ppm also had smaller but significant reductions in T-c. MA was unaffected by PTU. Overall, developmental exposure to moderate doses of an antithyroidal drug led to an apparent permanent reduction in T-c of adult offspring that was independent of changes in MA Published by Elsevier Inc.

Physical restraint of rodents is needed for nose-only exposure to airborne toxicants and is also used as a means of psychological stress. Hyperthermia is often observed in restrained rats, presumably as a result of impairments in heat dissipation. However, such a hyperthermic response should be dependent on the prevailing ambient conditions. To understand how ambient temperature (T(a)) affects the thermoregulatory response to restraint, core temperature (T(c)) and heart rate (HR) were monitored by telemetry in rats subjected to 1 h of physical restraint while T(a) was maintained at 14-30 °C in 2 °C increments. The T(c) of unrestrained rats was unaffected by T(a). During restraint, T(c) was elevated at ambient temperatures with the exception of 14 °C, at which the rats became mildly hypothermic. There was an inverse relationship between T(a) and HR in both unrestrained and restrained rats; however, HR was significantly elevated in restrained rats at all ambient temperatures except 22 and 24 °C. Heat loss from the tail, estimated from T(c) and tail skin temperature, was markedly reduced at all but the highest ambient temperatures in restrained rats. The data suggest that the T(a) limits of normothermia are narrowed in the restrained rat. That is, between 16 and 20 °C, the rat maintains a relatively stable T(c) that is slightly elevated above that of the unrestrained rat. At ambient temperatures above or below this range, the rat shows signs of hyperthermia and hypothermia, respectively. In contrast, the limits of normothermia for unrestrained rats range from 14 (or lower) to 30 °C. Overall, the ideal T(a) for restrained rats appears to be 20 °C and no higher than 22 °C for the thermoregulatory system to maintain a regulated T(c) in rats well adapted to physical restraint.

Physical restraint of rodents is needed for nose-only exposure to airborne toxicants and is also used as a means of psychological stress. Hyperthermia is often observed in restrained rats, presumably as a result of impairments in heat dissipation. However, such a hyperthermic response should be dependent on the prevailing ambient conditions. To understand how ambient temperature (T(a)) affects the thermoregulatory response to restraint, core temperature (T(c)) and heart rate (HR) were monitored by telemetry in rats subjected to 1 h of physical restraint while T(a) was maintained at 14-30 °C in 2 °C increments. The T(c) of unrestrained rats was unaffected by T(a). During restraint, T(c) was elevated at ambient temperatures with the exception of 14 °C, at which the rats became mildly hypothermic. There was an inverse relationship between T(a) and HR in both unrestrained and restrained rats; however, HR was significantly elevated in restrained rats at all ambient temperatures except 22 and 24 °C. Heat loss from the tail, estimated from T(c) and tail skin temperature, was markedly reduced at all but the highest ambient temperatures in restrained rats. The data suggest that the T(a) limits of normothermia are narrowed in the restrained rat. That is, between 16 and 20 °C, the rat maintains a relatively stable T(c) that is slightly elevated above that of the unrestrained rat. At ambient temperatures above or below this range, the rat shows signs of hyperthermia and hypothermia, respectively. In contrast, the limits of normothermia for unrestrained rats range from 14 (or lower) to 30 °C. Overall, the ideal T(a) for restrained rats appears to be 20 °C and no higher than 22 °C for the thermoregulatory system to maintain a regulated T(c) in rats well adapted to physical restraint.

1. The aims of the present study were to determine the cardiovascular effects of arachidonic acid (AA) and to investigate the peripheral mechanisms mediating these effects in haemorrhage-induced hypotensive rats. 2. Acute haemorrhage was induced by withdrawing a total volume of 2.2 mL blood/100 g bodyweight over a period of 10 min. Rats were then injected with 75-300 microg, i.c.v., AA and cardiovascular changes were monitored over the next 60 min. Plasma catecholamine and vasopressin levels, as well as plasma renin activity (PRA), were measured 10 min after injection of 150 microg AA in haemorrhage-induced hypotensive awake rats. In addition, rats were pretreated with saline (1 mL/kg, i.v.), the vasopressin V(1) receptor antagonist [beta-mercapto-beta,beta-cyclopentamethylenepropionyl(1),O-Me-Tyr(2),Arg(8)]-vasopressin (10 microg/kg, i.v.), the alpha(1)-adrenoceptor antagonist prazosin (500 microg/kg, i.v.), the non-specific angiotensin II receptor antagonist saralasin (250 microg/kg, i.v.) or a combination of these three antagonists 5 min before injection of AA (150 microg, i.c.v.). The effects of these antagonists on responses to AA were determined. 3. Arachidonic acid caused dose- and time-dependent increases in mean arterial pressure and heart rate and reversed hypotension in haemorrhaged rats. Haemorrhage itself produced an increase in plasma catecholamine and vasopressin levels, as well as PRA; injection of AA produced further increases in these parameters, ranging from 39-123%, under hypotensive conditions. Under hypotensive conditions, pretreatment of rats with all three receptor antagonists produced similar partial blockade of the pressor response to AA, but not the increase in heart rate. Moreover, combined administration of all three receptor antagonists prior to the i.c.v. injection of 150 microg AA completely abolished the pressor response to AA in haemorrhage-induced hypotensive rats. 4. These results indicate that centrally administered AA reverses hypotension by increasing blood pressure and heart rate in the hypotensive setting. The observed increases in plasma catecholamine and vasopressin levels, as well as PRA, mediate the pressor response to AA in haemorrhage-induced hypotensive rats.

Exhaustive exercise may generate oxidative stress in brain and reported findings are conflicting. Long term dietary restriction (DR) may be useful in the inhibiting of free oxygen radicals generated during exhaustive exercise in the brain of rat. Hence, in this study we evaluated beneficial effects of long term DR on the oxidative stress and antioxidant enzyme systems in brain cortex and lung in rats after different intensities of swimming exercise. Sprague-Dawley rats (60) were assigned as DR and ad libitum (AL) groups, and each group was further subdivided into three groups namely control (sedentery), submaximal exercise (endurance exercise) and maximal exercise (exhaustive swimming exercise) groups. Animals in the endurance exercise group swam 5 days/week for 8 weeks while exhaustive swimming group was subjected to an acute bout of exercise. With the increase in intensity of exercise, degree of lipid peroxidation (LP) and protein oxidation (PO) were also increased in DR and AL groups; however rate of increase was lower in DR group than AL group. Glutathione (GSH) and glutathione peroxidase (GSH-Px) activity were lower but glutathione reductase (GR) activity was higher in DR group compared to AL group in endurance and exhaustive swimming exercise. With increase in exercise intensity, GSH and GR enzyme activity decreased, whereas an increase was observed in GSH-Px enzyme activity. There was no difference in LP, PO, GSH and GR activity between DR and AL groups. GSH-Px activity in brain cortex was significantly lower in DR group than in AL group and sedentary rats. Results indicate that long term dietary restriction may protect against endurance and exhaustive swimming exercise-induced oxidative stress in rats by inhibiting oxidative stress.

Recently we demonstrated that centrally administrated melittin, a phospholipase A(2) (PLA(2)) activator, caused the pressor effect in normotensive, conscious rats. In the present study, we aimed to determine the cardiovascular effect of peripherally injected melittin and the involvement of the central cholinergic system on these effects in the normotensive conscious rats. For this reason, 250, 500 or 1000microg/kg doses of melittin were injected intraperitoneally to normotensive male Sprague Dawley rats. Melittin produced dose- and time-dependent increases in mean arterial pressure (MAP) and heart rate (HR). Both peripheral (5mg/kg; i.p.) and central (500microg; i.c.v.) pretreatment with indomethacin, nonselective inhibitor of cyclooxygenase (COX) 1 and 2, totally abolished cardiovascular effect of melittin. Intraperitoneal (i.p.) pretreatment with propranolol, a nonselective beta-adrenergic receptor blocker, completely abolished the tachycardic response to melittin. Also, the pressor effect of melittin was partially attenuated in these rats. In order to test the mediation of the central cholinergic system on the pressor and tachycardic effects of melittin, the rats were pretreated with atropine sulfate (10microg; i.c.v.), a cholinergic nonselective muscarinic receptor antagonist, mecamylamine (50microg; i.c.v.), a cholinergic nonselective nicotinic receptor antagonist, methyllycaconitine (10microg; i.c.v.) or alpha-bungarotoxin (10microg; i.c.v.), selective antagonists of alpha7 subtype nicotinic acetylcholine receptors (alpha7nAChRs) 15min prior to melittin (500microg/kg; i.p.) injection. Pretreatment with mecamylamine, methyllycaconitine or alpha-bungarotoxin partially diminished the pressor and tachycardic response to melittin in the normotensive conscious rats whereas pretreatment with atropine sulfate had no effect. In conclusion, our data demonstrate that peripherally administered melittin exerts a clear pressor and tachycardic effect by activating COX pathway. The activation of central cholinergic nicotinic receptors, predominantly alpha7nAChRs, appears to be involved in the pressor and tachycardic effects of the drug.

To investigate the appropriate surgical method that should be selected in the localized fecal peritonitis due to colonic injuries with 24 hours delay.Colonic injuries were performed in 35 rats and the repairs were carried out after 24 hours. Seven rats (%20) died of generalized peritonitis in this period. The remaining 28 rats in which fecal peritonitis were localized by surrounding organs, were randomized in two groups: colostomy (n=14) and primary anastomosis (n=14). Intraabdominal complications and 15 days mortality were assessed.The groups had similar results according to intraabdominal complications. The 15 days survival was 71.4 % for the colostomy group and 78.5 % for the anastomosis group (p=0.31)If the injured or perforated colon is surrounded by the organs and so the generalized peritonitis is avoided, primary anastomosis would have similar results with colostomy despite fecal contamination and prolonged intervention time.

The objective of this study was to determine the scolicidal effects of saline in different concentrations using different exposure times and to examine whether hypertonic saline can be used to irrigate the abdomen when there is a free intraperitoneal perforation of hydatid disease. Various concentrations of saline solutions (0.09%, 3.0%, 6.5%, 10%, 15%, 20%, 25%, 30%) were added to concentrated echinococcus granulosus sediments for the following times: 1, 2, 3, 4, 5, 10, 15, 30, 45, and 60 minutes. Normal (0.09%), 3.0%, and 6.5% saline resulted in high viability ratios after 60 minutes' exposure. Complete lethality for 10%, 15%, 20%, 25%, and 30% saline occurred at the end of 75, 10, 6, 3, and 3 minutes, respectively. During the second part of the study, 20 Sprague-Dawley rats were used for abdominal saline irrigation in four groups: 30% NaCl for 3 minutes; 20% NaCl for 6 minutes; intravenous isotonic dextrose water and furosemide plus 30% NaCl irrigation for 3 minutes; the same prophylactic therapy plus 20% NaCl irrigation for 6 minutes. Sodium and chloride values rose significantly (20–30%) shortly after hypertonic saline irrigation in each group (p < 0.01). Support with isotonic dextrose and furosemide before irrigation did not have any beneficial effect on biochemical values or mortality. The 24- and 48-hour mortality rates were 70% and 90%, respectively. These studies illustrate that the scolicidal effect of hypertonic saline is limited in low concentrations, but an increase in the concentration can augment its adverse effects. Peritoneal irrigation with hypertonic saline should be avoided for intraabdominal perforated hydatid disease. Therefore, we concluded that hypertonic saline is not a good scolicidal agent to prevent recurrence of hydatid disease.