The aim of the study was to investigate the mitigative effects of bisoprolol (BIS) in cadmium-induced myocardial toxicity on oxidative stress and its inhibitive effect on nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) signalling in rats. Male albino Wistar rats were assigned to control, Cd, BIS 2 (2 mg/kg b.w.) and BIS 8 (8 mg/kg b.w.) groups with nine rats in each. Over four weeks, the control group was administered 1% gum acacia, all other groups received 3mg/kg b.w. CdCl₂ dissolved in distilled water, and the BIS groups were additionally given bisoprolol in gum acacia. Blood samples were collected for biochemical estimations. Blood pressure and serum biomarker (lactate dehydrogenase, aspirate transaminase, alanine transferase and creatine kinase-MB, enzyme (superoxide dismutase, lipid hydroxy peroxidase, catalase and malondialdehyde), and tumour necrosis factor alpha (TNF-α) concentrations were measured. Western blot analysis was conducted for NF-κB and glutathione S-transferase (GST). After sacrificing the rats, cardiac tissue samples were examined histopathologically. Our findings pointed to a significant decrease (P < 0.05) in the studied serum biomarkers and levels of the relevant enzymes in the BIS 8 group compared to the Cd group. A significant decrease (P < 0.05) in NF-kB p65 expression and TNF-α levels was noted in the BIS 8 group relative to the BIS 2 and Cd groups, indicating a reduction at a higher dose. In microscopy, histopathological changes in the cardiac muscles of the BIS 8 group were evident compared to those of the Cd group. BIS seemed to have protective effects against cardiac injury induced by cadmium and could be considered a novel therapeutic drug and prognostic biomarker in the pathology of the many cardiovascular diseases caused by heavy metal intake.

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.

The purpose of this study was to investigate the protective effect of hydrogen-rich saline (HRS) against liver ischaemia-reperfusion combined resection injury. Eighteen miniature pigs were randomly divided into three groups: a sham operated group (sham group, laparoscopic liver ischaemia-reperfusion combined resection injury group (IRI group), and a hydrogen-rich saline intervention group (IRI + HRS group). Samples of hepatic tissue and serum were collected at the time of reperfusion and then 3 h, 1 d, and 3 d post reperfusion. Liver function, oxidative stress, autophagy-related mRNA genes, and protein expression were evaluated. Changes in cell and tissue ultrastructure were examined by transmission electron microscopy. Compared with the sham group, the level of autophagy of hepatocytes increased in the IRI and IRI + HRS groups, corresponding to high oxidative stress and severe liver function injury. Liver function, antioxidant content, autophagy levels, and liver injury were improved after intervention with HRS in the IRI + HRS group compared with the IRI group. Intervention with hydrogen-rich saline could exert a protective effect against liver ischaemia-reperfusion combined resection injury through the reduction of oxidative stress and hepatocyte autophagy.

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.

Dairy cows may infrequently give milk tinged with blood after calving, which is a condition termed haemolactia. Economic losses for dairy farmers are caused by cases of haemolactia because of the condemnation of such milk, potential contamination of good bulk tank milk with haemolactic milk, and need for veterinarian intervention. This study was performed to elucidate the oxidative status of dairy cows with haemolactia during the peripartum period. Plasma glutathione peroxidase, malondialdehyde (MDA) and superoxide dismutase concentrations along with serum vitamin A, C and E concentrations were determined as indices of oxidative stress. The sampled dairy cows comprised two haemolactic (n = 11 and n = 6) and two non-haemolactic (n = 11 and n = 6) groups. On the first day when haemolactia was identified in colostrum (at mean 2.1 days after parturition), a significantly increased concentration of plasma MDA was noted in the haemolactic group. During the prepartum period, low levels of serum vitamin E were continuously observed from prepartum week 4 to the parturition day but only in the haemolactic group. These results demonstrate that continuous low levels of serum vitamin E in the prepartum period may play a pivotal role as a requisite factor in the onset of haemolactia after calving.

Potential biomarkers for chronic seasonal heat stress in Kagoshima Berkshire pigs reared in the subtropical region were investigated by comparing the biomarker changes in the summer (a period of chronic heat stress) and winter (a thermoneutral period) seasons. Pigs were allocated to summer- and winter-finishing cohorts, 12 each. The evaluations included assessment of carcass traits and internal organs’ normality carried out at the time of slaughter, and measurement of biomarkers in whole blood: derivatives of reactive oxygen metabolites (d-ROMs) and biological antioxidant potential as markers of oxidative stress, and serum amyloid A and albumin/globulin (A/G) ratio as markers of acute and chronic inflammation, respectively. The summer-finished pigs reared under subtropical field conditions showed lower carcass quality than the winter-finished pigs, indicating a potential adverse effect of summer temperatures on the swine industry. Marginal changes were observed in d-ROMs and the A/G ratio between the summer- and winter-finishing cohorts. The results demonstrate that d-ROMs and the A/G ratio could be used as sensitive markers for heat stress under field conditions.

Several antidiabetic medications have been proposed as prospective treatments for cognitive impairments in type 2 diabetes patients, glibenclamide (GBC) among them. Our research aimed to evaluate the impact of GBC on hippocampal learning memory and inflammation due to enhanced neurotrophic signals induced by inhalation of sevoflurane. Rats (Sprague Dawley, both sexes) were assigned to four groups: a control (vehicle, p.o.), GBC (10 mg/kg b.w.; p.o.), low-dose sevoflurane and low-dose sevoflurane + GBC (10 mg/kg b.w.; p.o.) for 23 days. Terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) staining was performed to analyse the count of apoptotic cells and ELISA was conducted to assess the protein signals. A Western blot, a Y-maze test, and a Morris maze test were performed, and the results analysed. Blood and tissues were collected, and isolation of RNA was performed with qRT-PCR. The Morris maze test results revealed an improvement in the length of the escape latency on days 1 (P < 0.05), 2 (P < 0.01), 3, and 4 in the low-dose Sevo group. Time spent in the quadrant and crossing axis and the percentage of spontaneous alterations showed a substantial decrease in the low-dose Sevo group which received GBC at 10 mg/kg b.w. Significant increases were shown in IL-6 and TNF-α levels in the low-dose Sevo group, whereas a decrease was evident in the GBC group. Our results indicate that glibenclamide may be a novel drug to prevent sevoflurane inhalation-induced impaired learning and reduce brain-derived neurotrophic factor release, which may be a vital target for the development of potential therapies for cognitive deficits and neurodegeneration.

Foot rot in small ruminants is highly contagious, causes severe lameness, and impairs fertility and wool and meat production. It is usually treated with parenteral antibiotics, with attendant antibiotic resistance risk, and with bactericidal footbaths, potentially harmful to humans and the environment. An alternative treatment in sheep is proposed based on repeated topical ozonated ointment application. Its effectiveness and safety were evaluated by estimation of acute-phase response, biochemical indicators of organic damage, and antioxidant/oxidant balance (AOB). The study was conducted on ten sheep with Egerton scale 2–3 lesions. Ozone application was repeated every day for seven days. Blood was drawn first (T0) after foot cleaning and before ozonation, then (T1) seven days after the first ozone application, and finally (T2) four days after the last application. High clinical effectiveness was observed, with total recovery by 28 days from the start of treatment. A significant increase in antiradical activity was noted on the basis of a 2,2ʹ-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid) assay from 1.16 ± 0.04 μmolTe/mL at T0 to 1.23 ± 0.03 μmolTe/mL at T1, with a slight decrease in oxidative stress. Calculated on the basis of antiradical capacity, AOB was higher at T1 (130 ± 19%) and decreased to 110 ± 16% at T2. Calculated on the basis of reducing power, it was 169 ± 22% at T1 and 131 ± 17% at T2. These results indicated that the AOB is efficient enough to prevent oxidative organ injury and the applied doses of ozone are safe for animals.

The purpose of this study was to determine the effects of vitamin C supplementation on blood oxidative stress biomarkers and antibody response to vaccination in calves. Thirty-four clinically healthy 2 week old Japanese Black calves were randomly assigned to two groups. Seventeen calves formed the VC group which received 1,000 mg of vitamin C daily from 2 to 8 weeks of age, and the other 17 calves of the control group did not receive supplementation. All calves received an inactivated Histophilus somni vaccine at 4 and 8 weeks of age. Blood samples were taken at 2, 4, 8 and 12 weeks of age. The concentration of the serum reactive oxygen metabolites (d-ROMs), and the oxidative stress index (OSI), which is calculated from the d-ROMs and biological antioxidant potential, were significantly lower at 8 weeks of age in the VC group than in the control group (P < 0.05). The antibody titres to H. somni in the VC group were significantly higher than those in the control group at 12 weeks of age after the second vaccination (P < 0.05). Vitamin C supplementation to calves may reduce oxidative stress and enhance the antibody production after vaccination with H. somni.

The aim of this study was to evaluate potential protective effects of propolis on furan-induced hepatic damage by assessing the levels of malondialdehyde (MDA) and reduced glutathione (GSH), antioxidant enzyme activities, and histopathological changes in the liver. Albino Wistar rats were divided into six groups: a control, propolis-treated (100 mg/kg b.w./day), low-dose furan-treated (furan-L group; 2 mg/kg b.w./day), high-dose furan-treated (furan-H group; 16 mg/kg b.w./day), furan-L+propolis treated, and furan-H+propolis treated group. Propolis and furan were applied by gavage; propolis for 8 days, and furan for 20 days in furan-L groups and 10 days in furan-H groups. While MDA levels were elevated in furan-treated groups, levels of GSH and activities of antioxidant enzymes decreased (p < 0.001). The levels of MDA and GSH and activities of antioxidant enzymes were normal in the furan+propolis groups, especially in the furan-L+propolis group (p < 0.001). While the aspartate transaminase, alanine transaminase, alkaline phosphatase, and lactate pdehydrogenase activities were elevated in the furan-H treated group (p < 0.05 and p < 0.001), they were unchanged in the furan-L treated group. Histopathologically, several lesions were observed in the liver tissues of the furan-treated groups, especially in the higher-dose group. It was determined that these changes were milder in both of the furan+propolis groups. The results indicate that propolis exhibits good hepatoprotective and antioxidant potential against furan-induced hepatocellular damage in rats.