Ozone is not harmful itself; however, it directly oxidises biomolecules and produces radical-dependent cytotoxicity. Exposure to ozone is by inhalation and therefore the lungs develop the main anti-inflammatory response, while ozone has an indirect impact on the other organs. This study investigated the local and systemic effects of the ozone-associated inflammatory response.

Ozone is not harmful itself; however, it directly oxidises biomolecules and produces radical-dependent cytotoxicity. Exposure to ozone is by inhalation and therefore the lungs develop the main anti-inflammatory response, while ozone has an indirect impact on the other organs. This study investigated the local and systemic effects of the ozone-associated inflammatory response. Three groups each of 5 Wistar Han rats aged 6 months were exposed for 2h to airborne ozone at 0.5 ppm and a fourth identical group were unexposed controls. Sacrifice was at 3h after exposure for control rats and one experimental group and at 24 h and 48 h for the others. Lung and liver samples were evaluated for changes in expression of transforming growth factor beta 1, anti-inflammatory interleukin 10, pro-inflammatory tumour necrosis factor alpha and interleukin 1 beta and two nuclear factor kappa-light-chain-enhancer of B cells subunit genes. Total RNA was isolated from the samples in spin columns and cDNA was synthesised in an RT-PCR. Expression levels were compared to those of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and analysed statistically. All variables changed non-linearly over time comparing experimental groups to the control. Conspicuous expression changes in the subunit genes and cytokines were observed in both evaluated organs. Locally and systemically, inflammation responses to ozone inhalation include regulation of certain genes’ expression. The mechanisms are unalike in lungs and liver but ozone exerts a similar effect in both organs. A broader range of variables influential on ozone response should be studied in the future.

For many years, scientists have been pursuing research on skeletal muscle ageing both in humans and animals. Studies on animal models have extended our knowledge of this mechanism in humans. Most researchers agree that the major processes of muscle ageing occur in the mitochondria as the major energy production centres in muscle cells. It is believed that decisive changes occur at the enzymatic activity level as well as in protein synthesis and turnover ability. Deregulation of ion channels and oxidative stress also play significant roles. In particular, in recent years the free radical theory of ageing has undergone considerable modification; researchers are increasingly highlighting the partly positive effects of free radicals on processes occurring in cells. In addition, the influence of diet and physical activity on the rate of muscle cell ageing is widely debated as well as the possibility of delaying it through appropriate physical exercise and diet programmes. Numerous studies, especially those related to genetic processes, are still being conducted, and in the near future the findings could provide valuable information on muscle ageing. The results of ongoing research could answer the perennial question of whether and how we can influence the rate of ageing both in animals and humans.

Introduction: The goal of this study was to assess the influence of vaccination against enteric redmouth disease on oxidative stress biomarkers and antioxidant defence in the muscle tissue of rainbow trout (Oncorhynchus mykiss Walbaum) vaccinated against Yersinia ruckeri in the first and second month after immunisation. Material and Methods: Healthy fish were vaccinated orally with inactivated whole cells of a virulent strain of Y. ruckeri. One and two months after immunisation the muscle samples were collected. Results: No significant difference was noted in lipid peroxidation level in either the first or second month after vaccination, while aldehydic and ketonic derivatives of oxidatively modified proteins (OMB) in the vaccinated group were significantly lower in the second month compared to those in the first month after vaccination (P < 0.05). The content of ketonic derivatives of OMB in muscles in the first month after immunisation was higher compared to untreated control. All these culminated in a depletion of glutathione peroxidase (GPx) activity and low level of total antioxidant capacity (TAC). Conclusion: Correlations between catalase activity and lipid peroxidation and TAC confirmed the pivotal role of catalase in antioxidant defence during immunisation. From a broader perspective, it is suggested that immunisation of fish with Yersinia vaccine is associated with induced free radical formation and oxidative stress. Free radicals would therefore be at least partially responsible for the induction of both humoral and cellular elements of the immunity and increased protective immunity against Y. ruckeri infection.

Objective: The work aimed to determine the state of lipid peroxidation products and the activity of the antioxidant system in cats with aseptic inflammation and purulent-inflammatory processes of varying severity. Materials and Methods: The intensity of the process of lipid peroxidation- antioxidant system processes in blood plasma was evaluated using commercial kits. The level of diene conjugates (DC), the content of malondialdehyde (MDA), the level of medium-weight molecules were deter¬mined from lipid peroxidation indices. The state of antioxidant protection was assessed by indi¬cators of superoxide dismutase (SOD) activity, catalase (CT), ceruloplasmin (CP) concentration, glutathione peroxidase activity, glutathione reductase (GLR), and total antioxidant activity (AOA). Results: With aseptic inflammation in the blood of cats, a slow activation of peroxidation reactions occurred. The DC indicator increased by 1.4 times, the SOD level rose by 1.38 times, the amount of GLR by 1.04 times, and the activation of total AOA by 9.06. In sepsis, the values of DC, MDA, and medium-weight molecules increased by 4.4, 8.4, and 8.8 times, respectively. With abscesses in the blood of cats, an increase in CT, CP, and GLR is observed against a background of a decrease in glutathione peroxidase. With purulent wounds, the total AOA of plasma increases by 2.5 times; with abscesses, the total AOA increases by 1.9 times, and with sepsis, it decreases by 1.5 times. Conclusion: With surgical infections in cats, deep biochemical changes or irreversible biochemical changes (in sepsis) occur that indicate a significantly enhanced catabolic orientation of metabolic processes and the accumulation of toxic metabolites, which leads to damage and a decrease in tissue regenerative capacity. [J Adv Vet Anim Res 2021; 8(2.000): 210-217]

Thirty horses were randomly assigned to 1 of 5 groups. All horses were anesthetized and subjected to ventral midline celiotomy, then the large colon was exteriorized and instrumented. Colonic arterial blood flow was reduced to 20% of baseline (BL) and was maintained for 3 hours. Colonic blood flow was then restored, and the colon was reperfused for an additional 3 hours. One of 5 drug solutions was administered via the jugular vein 30 minutes prior to colonic reperfusion: group 1, 0.9% NaCl; group 2, dimethyl sulfoxide: 1 g/kg of body weight; group 3, allopurinol: 25 mg/kg; group 4, 21-aminosteroid U-74389G: 10 mg/kg; and group 5, manganese chloride (MnCl2): 10 mg/kg. Hemodynamic variables were monitored and recorded at 30-minutes intervals. Systemic arterial, systemic venous (SV), and colonic venous (CV) blood samples were collected for measurement of blood gas tensions, oximetry, lactate concentration, PCV, and plasma total protein concentration. The eicosanoids, 6-keto prostaglandin F1alpha, prostaglandin E2, and thromboxane B2, were measured in CV blood, and endotoxin was measured in CV and SV blood. Full-thickness biopsy specimens were harvested from the left ventral colon for histologic evaluation and determination of wet weight-to-dry weight ratios (WW:DW). Data were analyzed, using two-way ANOVA for repeated measures, and statistical significance was set at P < 0.05. Heart rate, mean arterial pressure, and cardiac output increased with MnCl2 infusion; heart rate and cardiac output remained increased throughout the study, but mean arterial pressure returned to BL values within 30 minutes after completion of MnCl2 infusion. Other drug-induced changes were not significant. There were significant increases in mean pulmonary artery and mean right atrial pressures at 2 and 2.5 hours in horses of all groups, but other changes across time or differences among groups were not observed. Mean pulmonary artery pressure remained increased through 6 hours in all groups, but mean right atrial pressure had returned to BL values at 3 hours. Mean colonic arterial pressure was significantly decreased at 30 minutes of ischemia and remained decreased through 6 hours; however, by 3.25 hours it was significantly higher than the value at 3 hours of ischemia. Colonic arterial resistance decreased during ischemia and remained decreased throughout reperfusion in all groups; there were no differences among groups for colonic arterial resistance. Colonic venous PO2, oxygen content, and pH decreased, and PCO2 and lactate concentration increased during ischemia but returned to BL values during reperfusion. Compared with BL values, colonic oxygen extraction ratio was increased from 0.5 to 3 hours. By 15 minutes of reperfusion, colonic oxygen extraction ratio had decreased from the BL value in all groups and either remained decreased or returned to values not different from BL through 6 hours. Colonic venous 6-keto prostaglandin F1alpha and prostaglandin E2 concentrations increased during ischemia, but returned to BL on reperfusion; there were no changes in thromboxane2 concentration among or within groups. Endotoxin was not detected in CV or SV blood after ischemia or reperfusion. There were no differences among or within groups for these variables. Low-flow ischemia and reperfusion (I-R) of the large colon caused mucosal injury, as evidenced by increases in percentage of surface mucosal disruption, percentage depth of mucosal loss, mucosal hemorrhage, mucosal edema, mucosal interstitial-to-crypt ratio, mucosal neutrophil index, submucosal venular neutrophil numbers, and mucosal cellular debris index. There was a trend (P = 0.06) toward greater percentage depth of mucosal loss at 6 hours in horses treated with dimethyl sulfoxide, compared with the vehicle control solution. There were no differences in the remainder of the histologic variables among groups. Full-thickness and mucosal WW:DW increased with colonic I-R, but there were no differences among groups. There was a trend (P = 0.09) toward neutrophil accumulation, as measured by myeloperoxidase activity, in the lungs after colonic I-R, but there were no differences among groups. There was no change in lung WW:DW after colonic I-R. There were no beneficial effects of drugs directed against oxygen-derived free radical-mediated damage on colonic mucosal injury associated with low-flow I-R. Deleterious drug-induced hemodynamic effects were not observed in this study.

Sheets of mucosa from the jejunum of healthy horses were mounted in incubation chambers and bathed with Krebs-ringer bicarbonate solution. Changes in tissue function and histologic appearance were compared after the following conditions: (1) control conditions for 30 minutes with 95% O2/5% CO2 in the gas phase; (2) same conditions as control, except incubation with superoxide dismutase (300 U/ml) during the last 18 minutes; (3) anoxia for 15 minutes with 95% N2/5% CO2, followed by reoxygenation for 15 minutes; (4) same conditions as 3, except incubation with superoxide dismutase during reoxygenation; and (5) anoxia for 30 minutes. Anoxia reduced the accumulation of radiolabeled L-alanine and caused cell swelling, as indicated by an increase in tissue water and tissue Na contents. Reoxygenation improved the tissue's ability to accumulate L-alanine, but tissue swelling continued after this treatment. Tissue Na content and L-alanine accumulation were restored to control values by reoxygenation with superoxide dismutase in the bathing medium. The grade of structural damage, as indicated by separation of eptihelial cells from villi, was equally severe after all, but control, conditions. Superoxide dismutase had no effect on the tissue control conditions. Results of this study suggest that superoxide radicals are involved in the pathogenesis of reperfusion injury in equine jejunal mucosa and that this may be of clinical importance in cases of small intestinal strangulation obstruction.

The objective of this study was to evaluate the ability of a long-term antioxidant-supplemented diet to regulate the oxidative stress and general health status of dogs involved in animal-assisted intervention (AAI) programs. Oxidative stress is a consequence of the accumulation of reactive oxygen species (ROS). Exercise-induced oxidative stress can increase muscle fatigue and fiber damage and eventually leads to impairment of the immune system. A randomized, placebo-controlled, crossover clinical evaluation was conducted with 11 healthy therapy dogs: 6 females and 5 males of different breeds and with a mean age of 2.7 ± 0.8 y (mean ± SEM). The dogs were divided into 2 groups, 1 fed a high quality commercial diet without antioxidants (CD) and the other a high quality commercial diet supplemented with antioxidants (SD) for 18 wk. After the first 18 wk, metabolic parameters, reactive oxygen metabolite-derivatives (d-ROMs), and biological antioxidant potential (BAP) levels were monitored and showed a significant reduction of d-ROMs, triglycerides, and creatinine values in the SD group (P < 0.05) and a significant increase in amylase values in the CD group (P < 0.01). At the end of this period, groups were crossed over and fed for another 18 wk. A significant decrease in amylase and glutamate pyruvate transaminase (GPT) values was observed in the CD and SD group, respectively (P < 0.05). In conclusion, a controlled, balanced antioxidant diet may be a valid approach to restoring good cell metabolism and neutralizing excess free radicals in therapy dogs.

Generation of free radicals and the ability of various antioxidants to attenuate radical production in freshly procured cancellous bone specimens was investigated, using spin-trapping and electron spin resonance (ESR) techniques. Seven core cancellous bone specimens, 10 mm long and 7.9 mm in diameter, were obtained using aseptic technique, from the proximal portion of the humerus of 9 adult mixed-breed dogs. One core cancellous bone specimen from each dog was incubated in spin trap alpha-phenyl-N-tert-butylnitrone in Eagle's minimum essential medium and served as a control. The other 6 specimens from each dog were incubated in alpha-phenyl-N-tert-butylnitrone/Eagle's minimum essential medium plus 1 of the following antioxidants: superoxide dismutase, catalase, superoxide dismutase/catalase, indomethacin, allopurinol, or deferoxamine mesylate. All specimens were incubated at 26 C for 90 minutes, then frozen at -20 C until they were prepared for analysis by ESR spectroscopy. Each specimen was thawed, homogenized, and extracted in a low-dielectric organic solvent prior to obtaining an ESR spectrum which was analyzed for hyperfine splitting constants to identify radicals. Each first-derivative spectrum was digitally double-integrated to obtain an area: these areas were used to compare intensities of the spin. For each treatment group, the areas from the treated specimens were compared with the areas from the control specimens, using a paired t-test. Significance was accepted at P less than or equal to 0.05. Spin adducts were detected in all cancellous bone specimens. Specimens incubated in deferoxamine (P = 0.0017) and superoxide dismutase/catalase (P = 0.0452) had significantly smaller areas than did control specimens. The areas for the other treatment groups did not differ significantly from controls. Our results substantiate free radical production in freshly procured cancellous bone specimens and that radical formation is attenuated by in vitro incubation with deferoxamine or superoxide dismutase/catalase.

The formylated peptide, N-formyl-methionyl-leucyl-phenylalanine, at concentration of 0.22 micromolar, failed to stimulate canine neutrophils to produce adequate amounts of superoxide. Furthermore, addition of cytochalasin B did not augment superoxide generation appreciably.