Oxidative Stress In Cats Research Articles

Moderate to advanced periodontitis contributes to increased oxidative stress in cats: a case-control study

BackgroundPeriodontal diseases are the most frequently diagnosed problem in cats. It has been well-established that periodontal diseases could not only cause various oral health issues but could also contribute to systemic diseases. Oxidative stress is a possible link between systemic diseases and periodontitis. Our study aimed to illustrate the influence of periodontitis on oxidative stress development in cats. Furthermore, the changes in the bacterial flora of the gums were investigated.MethodsBased on the clinical and laboratory examinations, fifty cats were divided into two groups normal (n = 25) and moderate to advanced periodontitis (n = 25). Serum total antioxidant capacity (TAC), total oxidant status (TOS), reduced (GSH) and oxidized glutathione (GSSG) were measured. In addition, samples were taken from the subgingival plaques of all cats for bacterial culture.ResultsSerum TOS, GSSG, GSSG to GSH ratio, and oxidative stress index (OSI), calculated as the ratio of TOS to TAC in cats with periodontal disease were significantly higher, and TAC was significantly lower (p < 0.05) compared with controls. The results of bacterial culture indicated that the number of isolated bacterial colonies is higher in patients than in the control group. Additionally, the analysis of these data showed a positive association between periodontal index and oxidative stress.ConclusionsOur results revealed that periodontitis in cats is related to a main oxidative stress. Furthermore, oxidant factors such as TOS and OSI, compared to antioxidant factors, may better indicate the presence of oxidative stress conditions in patients with periodontitis.

Blood plasma and urinary biomarkers of oxidative stress in cats with urethral obstruction

BackgroundThis study aimed to investigate variations of the oxidative status in cats affected by urethral obstruction (UO) under Feline Idiopathic Cystitis (FIC) and Bacterial Cystitis (BC), in comparison with a group of healthy subjects. In both groups, the levels of several markers (either direct or indirect) indicative of the oxidative attack and of the antioxidant response were analyzed on plasma and urine samples. In particular, the plasma samples were evaluated for nitric oxide (NO), hydroperoxides derived by reactive oxygen activity (d-ROMs test), superoxide anion (O2−), glutathione peroxidase activity (GPx), superoxide dismutase activity (SOD), and ferric reducing antioxidant power (FRAP test); while on urine the levels of NO, d-ROMs, FRAP, SOD, malondialdehyde (MDA) and 8-hydroxydeoxyguanosine (8-OHdG) were measured. Urine of UO patients was also subjected to urine-culture test.ResultsThe analytical data on plasma showed that UO, independently of the FIC or BC etiology, induced the insurgence of oxidative stress conditions at the systemic level. In the urine of the UO patients, except for SOD that increased, the markers of redox status were markedly decreased due probably their compromised filtration, thus suggesting involvement of renal function (assessed also by the high levels of plasma creatinine and proteinuria) with no oxidative damage of the lower urinary tract. Moreover, the adoption of a novel oxidative stress index’ (OSI) allowed to establish, by means of a numerical value, the different degrees of oxidative stress conditions for single UO patients, both in terms of oxidative attack and antioxidant response.ConclusionsFeline urethral obstruction, induced by Idiopathic Cystitis and Bacterial Cystitis, causes oxidative stress conditions at the systemic level that do not interest the lower urinary tract. Despite to the high variability of the profiles of oxidative stress indexes both in healthy and UO patients, the determination of OSI made possible the evaluation of their single degrees of oxidative stress. Possibly the results of this investigation can be compared with those of correspondent pathologies both in humans and in other animal species.

8-Hydroxy-2'-deoxyguanosine and malondialdehyde in plasma and their association with disease severity in 20 cats with chronic kidney disease.

Oxidative stress is associated with the development and progression of chronic kidney disease (CKD) in humans. The aim of this study was to evaluate the concentrations of oxidative stress markers, 8-hydroxy-2'-deoxyguanosine (8-OHdG) and malondialdehyde (MDA), in the plasma and urine of cats with different stages of CKD. Plasma and urine samples were collected from cats with CKD that were referred to the Veterinary Medical Center of the University of Tokyo between April 2019 and October 2022. Plasma and urine samples were collected from healthy cats (n = 6 at most), cats with stage 2 CKD (n = 8) and stage 3-4 CKD (n = 12), and cats with idiopathic cystitis (disease control, n = 5). Plasma and urine concentrations of 8-OHdG and MDA were measured using ELISA and thiobarbituric acid reactive substances assay kits, respectively. The median plasma 8-OHdG concentrations were 0.156 ng/ml (<0.125-0.210 ng/ml) in the healthy group, <0.125 ng/ml (range <0.125 ng/ml) in the idiopathic cystitis group, 0.246 ng/ml (range 0.170-0.403 ng/ml) in cats with stage 2 CKD and 0.433 ng/ml (range 0.209-1.052 ng/ml) in cats with stage 3-4 CKD. Concentrations in stage 3-4 CKD were significantly higher than those in the healthy and disease control groups. Plasma MDA concentrations were low in the healthy and disease control groups and significantly higher in cats with stage 3-4 CKD. In every cat with CKD, plasma 8-OHdG and MDA concentrations were positively correlated with plasma creatinine concentrations (8-OHdG, rs = 0.68; MDA, rs = 0.67). Urinary 8-OHdG/urinary creatinine (u-CRE) and urinary MDA/u-CRE levels did not differ significantly between the groups; however, it was difficult to evaluate them because of the small sample size. This report shows that plasma 8-OHdG and MDA concentrations increase with the severity of feline CKD. These markers may be useful for assessing oxidative stress in cats with CKD.

Evaluation of Prophylactic and Therapeutic Effects of Silymarin on Phenobar- bital-Induced Hepatotoxicity in Cats

BACKGROUND: Phenobarbital is one of the most commonly used drugs to treat epilepsy and other seizure disorders in dogs and cats. Hepatotoxicity following phenobarbital administration is dose-dependent. OBJECTIVES: The present study aimed to evaluate the protective action of silymarin on phenobarbital-in- duced hepatotoxicity in cats. METHODS: For this purpose, twenty-four healthy adult cats were randomly allotted to four equal groups. Cats in group A were given phenobarbital with dosage 16 mg/kg orally for 28 days; group B received silymarin (30 mg/kg/day for twenty-eight days) orally concurrent with phenobarbital; groups C and D were treated like group B, but silymarin was administered 3 and 48 h after administration of phenobarbital, respectively, and continued up to twenty-eight days. The serum concentrations of alanine aminotransferase, aspartate amino- transferase, alkaline phosphatase, lactate dehydrogenase, total and direct bilirubin, blood urea nitrogen and creatinine were measured before administration of phenobarbital and after 24 h, 72 h and 28 days. RESULTS:Phenobarbital elevated significantly serum concentrations of liver enzymes (in all cases), and total and direct bilirubin in two cats of group A, after 24 h (P 0.05), while in group D, levels of serum enzyme activities (in 4 cases) were higher than the normal values (P<0.001). CONCLUSIONS: The results showed that silymarin can protect liver tissue against oxidative stress in cats with phenobarbital intoxication especially in the first 3 h post-exposure.

Urinary F2 -Isoprostanes in Cats with International Renal Interest Society Stage 1-4 Chronic Kidney Disease.

BackgroundF2‐isoprostanes, a biomarker of oxidant injury, increase with advancing chronic kidney disease (CKD) in humans. In cats, the relationship between CKD and oxidative stress is poorly understood.ObjectivesTo determine whether cats with advancing CKD have increasing urinary F2‐isoprostanes.AnimalsControl cats without evidence of CKD (≥6 years old; n = 11), and cats with IRIS stage 1 (n = 8), 2 (n = 38), 3 (n = 21), and 4 (n = 10) CKD.MethodsThis was a prospective observational study. Urinary F2‐isoprostanes (specifically free 15‐F2t‐isoprostanes) normalized to urine creatinine (IsoPs) were compared among groups and tested for correlations with blood pressure, proteinuria, serum creatinine concentration, and urine specific gravity. The IsoPs also were compared between cats with and without hypertension or proteinuria, and in cats fed predominantly standard versus renal diets.ResultsUrinary IsoPs were increased, but not significantly, in cats with stage 1 CKD (median 263 pg/mg creatinine; range, 211–380) compared to controls (182 pg/mg; range, 80–348) and decreased significantly from stage 1 through advancing CKD (stage 2, 144 pg/mg; range, 49–608; stage 3, 102 pg/mg; range, 25–158; stage 4, 67 pg/mg; range, 26–117; P < .01). Urinary IsoPs were inversely correlated with serum creatinine (r = −0.66, P < .0001).Conclusion and Clinical ImportanceUrinary IsoPs are significantly higher in early CKD (stage 1) compared to cats with more advanced CKD. Additional studies are warranted to characterize oxidative stress in cats with stage 1 CKD and determine whether early antioxidant treatments have a protective effect on CKD progression.

Serum biomarkers of oxidative stress in cats with feline infectious peritonitis

The purpose of this study was to elucidate the possible presence of oxidative stress in cats naturally affected by feline infectious peritonitis (FIP) by investigating two antioxidant biomarkers in serum: paraoxonase-1 (PON1) and total antioxidant capacity (TAC). PON1 was measured by spectrophotometric assays using three different substrates: p-nitrophenyl acetate (pNA), phenyl acetate (PA) and 5-thiobutil butyrolactone (TBBL), in order to evaluate possible differences between them. The PA and TBBL assays for PON1 and the assay for TAC were validated, providing acceptable precision and linearity although PA and TAC assays showed limit of detection higher than the values found in some cats with FIP. Cats with FIP and other inflammatory conditions showed lower PON1 values compared with a group of healthy cats with the three assays used, and cats with FIP showed significant decreased TAC concentrations. This study demonstrated the existence of oxidative stress in cats with FIP.

Evaluation of Prophylactic and Therapeutic Effects of Silymarin on Diazepam-Induced Hepatotoxicity in Cats

Problem statement: Diazepam is commonly administered for seizure control and appetite stimulant in cats. Cats may develop acute fatal hepatic necrosis after receiving oral diazepam for several days. The aim of this study was to detect the protective action of silymarin on diazepam-induced hepatotoxicity in cats. Approach: About 25 healthy cats were randomly allotted to five equal groups. Animals in Group A were given diazepam (repeated dose 2.5 mg kg-1, p.o. q 12 h for 4 days); Group B consisted of cats that received silymarin (30 mg kg-1, p.o. q 12 h for 4 days) concurrent with diazepam administration; Group C were received silymarin like Group B, but 24 h after diazepam administration; Group D were received silymarin like Group C, but 48 h after diazepam administration; Group E were received silymarin like Group D, but 72 h after diazepam administration. The serum concentrations of Alanine Amino Transferase (ALT), Aspartate Aminotransferase (AST), Alkaline Phosphatase (ALP), Lactate Dehydrogenase (LDH) and total and direct bilirubin were measured before diazepam administration and 24, 48, 72 and 96 h later as indices of liver injury. Results: Repeated oral administration of diazepam significantly elevated serum concentrations of ALT, AST, ALP, LDH and total and direct bilirubin in cats of Group A, after 48 h. In both the Groups (B and C) receiving silymarin, levels of serum enzyme activities and total and direct bilirubin remained within the normal values, but the Group D and E which received silymarin 48 h and 72h later, levels of serum enzyme activities and total and direct bilirubin were increased with comparison to before diazepam administration. Conclusion: It was concluded that silymarin can protect liver tissue against oxidative stress in cats with diazepam intoxication particular in the first 24 h after exposure.

Evaluation of prophylactic and therapeutic effects of silymarin on mebendazole-induced hepatotoxicity in cats

The aim of this study was to determine the protective action of silymarin on mebendazole-induced hepatotoxicity in cats. Twenty five healthy cats were randomly allotted into five equal groups. Cats in group A were given mebendazole (single dose 200 mg⁄kg, p.o.); group B consisted of cats that received silymarin (single dose 30 mg⁄kg, p.o.) concurrent with mebendazole administration; groups C, D and E were treated as group B, but silymarin was administered 2, 12 and 24 h after mebendazole administration, respectively. The serum concentrations of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and total and direct bilirubin were measured before mebendazole administration and 2, 12, 24 and 72 h later as indices of liver injury. A single oral administration of mebendazole significantly elevated serum concentrations of ALT, AST, ALP, LDH (in all cases), and total and direct bilirubin in one cat in group A, after 24 h (P < 0.05). In groups B and C, levels of serum enzyme activities and total and direct bilirubin remained within normal values, but in group D, levels of serum enzyme activity (in four cases) were higher than normal values and total and direct bilirubin remained within the normal range. In group E, levels of serum enzyme activities (in all cats) and total and direct bilirubin (in one cat) were higher than normal values. In conclusion, silymarin can protect liver tissue against oxidative stress in cats with mebendazole intoxication particularly in the first 2 h after exposure.

Evaluation of prophylactic and therapeutic effects of silymarin andN-acetylcysteine in acetaminophen-induced hepatotoxicity in cats

Cats most commonly receive toxic amounts of acetaminophen (APAP) because owners medicate them without consulting a veterinarian. The aim of this study was to compare the hepatoprotective action of silymarin and N-acetylcysteine (NAC) against APAP poisoning. Twenty healthy cats were randomly allotted to five equal groups. Animals in group A were given APAP (single dose 150 mg/kg, p.o.); groups B and C consisted of cats that received NAC (100 mg/kg, p.o.) or silymarin (30 mg/kg, p.o.) concurrent with APAP administration respectively; groups D and E were treated like groups B and C, respectively, but 4 h after APAP administration. The serum concentrations of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), methemoglobin, and total and direct bilirubin were measured before APAP administration and 4, 24, and 72 h later. A single oral administration of APAP significantly elevated serum concentrations of ALT, AST, ALP, LDH, methemoglobin, and total and direct bilirubin. In both the groups receiving APAP plus NAC or silymarin, levels of serum enzyme activities, methemoglobin, and total and direct bilirubin remained within the normal values. It was concluded that silymarin as well as NAC can protect liver tissue against oxidative stress in cats with an APAP intoxication.

Antioxidant status and biomarkers of oxidative stress in cats with diabetes mellitus

Increasing evidence implicates oxidative damage in the progression and pathologic complications of human diabetics. This study assessed antioxidant status and oxidative stress in cats with diabetes mellitus (DM). Antioxidant status was measured in diabetic (n = 10) and control (n = 10) cats by HPLC of vitamin E isomers, reduced (GSH) and oxidized glutathione (GSSG), and calculation of the GSH:GSSG ratio. Biomarkers of protein, lipid and DNA peroxidation (fructosamine, isoprostanes and Comet assay, respectively), and neutrophil function evaluated oxidative stress. Correlation between glycemic control and antioxidant status/ oxidative stress was also investigated. A diabetic index was generated using clinical signs, body condition score, insulin dose, fructosamine, fasted blood glucose and urinary glucose and ketones. Alpha tocopherol was increased (DM = 0.11 μg/mL, controls = 0.06 μg/mL; p = 0.0012) and gamma tocopherol was decreased (DM = 0.03 μg/mL, controls = 0.05 μg/mL; p = 0.0065) in diabetic vs. control cats. There was no difference in the GSH:GSH ratio between groups. Predictably, fructosamine was greater in diabetic vs. control cats (DM = 447 μmol/L, controls = 204 μmol/L; p < 0.0001). Antioxidant status/oxidative stress was not associated with glycaemic control in diabetic cats. Despite strong association of DM with oxidative stress in humans, this simple relationship is not found in diabetic cats. They have both increased and decreased parameters of systemic oxidative stress compared with control cats. This may be due to higher levels of antioxidants in feline therapeutic diets, the relatively short duration of disease in cats compared with humans, or other factors.

Oxidative stress during acute FIV infection in cats

Oxidative stress is thought to contribute to the pathogenesis of HIV infection in humans. For example, CD4 + T cells are particularly affected in HIV patients and oxidative stress may also contribute to impairment of neutrophil function in HIV/AIDS patients. Since cats infected with FIV develop many of the same immunological abnormalites as HIV-infected humans, we investigated effects of acute FIV infection on oxidative stress in cats. Cats were infected with a pathogenic strain of FIV and viral load, changes in neutrophil number, total blood glutathione, malondiadehye, antioxidant enzyme concentrations, and reduced glutathione (GSH) concentration in leukocytes were measured sequentially during the first 16 weeks of infection. We found that superoxide dismutase and glutathione peroxidase concentrations in whole blood increased significantly during acute FIV infection. In addition, neutrophil numbers increased significantly during this time period, though their intracellular GSH concentrations did not change. In contrast, the numbers of CD4 + T cells decreased significantly and their intracellular GSH concentration increased significantly, while intracellular GSH concentrations were unchanged in CD8 + T cells. However, by 16 weeks of infection, many of the abnormalities in oxidative balance had stabilized or returned to pre-inoculation values. These results suggest that acute infection with FIV causes oxidative stress in cats and that CD4 + T cells appear to be preferentially affected. Further studies are required to determine whether early treatment with anti-oxidants may help ameliorate the decline in CD4 + T cell number and function associated with acute FIV infection in cats.

Dietary Supplements of Vitamins E and C and β-Carotene Reduce Oxidative Stress in Cats with Renal Insufficiency

Oxidative stress may contribute to the progression of chronic renal failure. In this study, cats with spontaneous renal insufficiency were fed a dry cat food supplemented with the antioxidants vitamins E and C, and beta-carotene for 4 weeks. When compared with healthy cats, cats with renal insufficiency had a tendency to oxidative stress. The antioxidant supplements significantly reduced DNA damage in cats with renal insufficiency as evidenced by reduced serum 8-OHdG and comet assay parameters. Therefore, supplements of vitamins E and C and beta-carotene as antioxidants may be beneficial to cats with renal disease.

Increase in plasma lipid peroxide in cats fed a fish diet.

Plasma lipid peroxide levels were examined in cats. Plasma lipid peroxide levels in 3 of 4 clinical cases which had been fed raw fish were higher than those in normal cats. When healthy cats were put on a raw fish diet in controlled conditions, a remarkable increase in plasma lipid peroxide was observed. This increase occurred within 1 to 3 weeks in cats without obvious clinical disorders. We also showed that a continuous raw fish diet is necessary to cause the increase, but the increase was transient and restored in spite of a continuous raw fish diet, indicating the development of an unidentified antioxidant process. Our results clearly indicate that intake of foods high in polyunsaturated fatty acid can induce oxidative stress in cats.