DNA damage and effects on antioxidative enzymes in earthworm (Eisenia foetida) induced by atrazine

To evaluate atrazine (2-chloro-4-ethylamino-6-isopropylamino-1, 3, 5-triazine) ecotoxicology in soil, the effect of atrazine on the activity of antioxidative enzymes (superoxide dismutase, SOD; catalase, CAT; and guaiacol peroxidase, POD) and DNA damage induced by atrazine were investigated in earthworms. Atrazine was added to artificial soil at rates of 0, 2.5, 5 and 10 mg per kg of soil. Earthworm tissues exposed to each treatment were collected on the 7th, 14th, 21st, and 28th day of the treatment. Compared to the controls, the CAT activity was stimulated at 2.5 mg kg⁻¹ treatment except on the 14th day, and inhibited at 5, 10 mg kg⁻¹ atrazine except 5 mg kg⁻¹ on the 28th day and 10 mg kg⁻¹ on the 21st day; the overall SOD activity was inhibited, while the POD activities were stimulated by all atrazine concentrations in 28 days. The olive tail moments of single-cell gel electrophoresis of coelomocytes, as an indication of DNA damage, were increased after treatment with different doses of atrazine on the 7th, 14th, 21st, and 28th day, and significant differences were found compared to the controls. In conclusion, atrazine induces oxidative stress and DNA damage on earthworms, and the adverse effects may be the important mechanisms of its toxicity to earthworms.     

Trans-10, cis-12 conjugated linoleic acid modulates phagocytic responses of canine peripheral blood polymorphonuclear neutrophilic leukocytes exposed to Clostridium difficile toxin B

Trans-10, cis-12 conjugated linoleic acid (t10c12-CLA) has been reported to enhance phagocyte function. Clostridium difficile toxin B (TcdB) has been known to inhibit Ras-homologous (Rho) guanosine triphosphatases (GTPases) which play essential roles in neutrophil immune functions. Here, we examined whether in vitro treatment with t10c12-CLA modulates the filamentous actin (F-actin) polymerization, phagocytic capacity, and oxidative burst activity (OBA) of canine peripheral blood polymorphonuclear neutrophilic leukocytes (PMNs) exposed to TcdB. Treatment with t10c12-CLA, but not linoleic acid, enhanced PMN F-actin polymerization, phagocytic capacity, and OBA, while TcdB suppressed these functions. t10c12-CLA reversed the suppressive effects of TcdB on these PMN functions. t10c12-CLA stimulated F-actin polymerization regardless of whether phagocytosis was stimulated by microspheres but only elevated OBA when microspheres were added. We asked whether the effects of t10c12-CLA were associated with changes in the activation of the Rho GTPase Cdc42. Treatment with t10c12-CLA augmented Cdc42 activity in both TcdB-treated and TcdB-naive PMNs during phagocytosis. Thus, t10c12-CLA up-regulates PMN phagocytic responses attenuated by TcdB. This effect is associated with an increase in actin polymerization and may involve the activation of Cdc42.     

Immunolocalization of INSL3 in dog foetal Leydig cells and the LGR8 receptor in the gubernaculum testis

Oxidative stress parameters; thiobarbituric acid reaction substances (RBC-TBARS), catalase (RBC-CAT) and reduced glutathione (RBC-GSH)) and the intraerythrocytic concentrations of electrolytes; sodium and potassium (RBC-Na and RBC-K) were determined in 18 well- controlled (WC) and 22 poorly-controlled diabetic mellitus (DM). Dogs with DM had significant higher blood glucose concentration (P < 0.001), haemoglobin A1c (P < 0.01) and fructosamine (P < 0.001) compared to normal healthy dogs (n = 19). Diabetic dogs in both groups had higher RBC-CAT (P < 0.05) while RBC-TBARS were higher significantly only in poorly-controlled DM group (P < 0.05). The RBC-K was significantly higher in both DM groups (P < 0.001). No changes in RBC-GSH and RBC-Na were found between DM and control healthy dogs. By linear regression analysis, the relationship were found between degree of diabetic mellitus and RBC-CAT, RBC-TBARS, RBC-Na and RBC-K. The relationship was also found between oxidative stress parameters and intraerythrocytic K⁺. The results suggest that in diabetic dogs, oxidative stress occurs which related to the severity of disease and may affect potassium homeostasis.     

Glutathione, Cysteine, and Ascorbate Concentrations in Clinically Ill Dogs and Cats

Background: Oxidative stress plays a role in the pathogenesis of many systemic diseases. Hospitalized human patients are glutathione, cysteine, and ascorbate deficient, and antioxidant depletion has been correlated with poor clinical outcome. To date little is known about antioxidant concentrations in hospitalized veterinary patients. The purpose of this study was to determine whether ascorbate, cysteine, or glutathione depletion is present in ill dogs and cats compared with healthy controls.
Hypothesis: Clinically ill dogs and cats would be antioxidant depleted, and depletion would correlate with illness severity and clinical outcome.
Animals: Clinically ill client-owned dogs (n = 61) and cats (n = 37), healthy control dogs (n = 37) and cats (n = 33).
Methods: Prospective, observational, case control study. Erythrocyte reduced glutathione, plasma cysteine, and plasma ascorbate were quantified using high-performance liquid chromatography.
Results: Clinically ill dogs had significantly lower erythrocyte glutathione concentrations (1.22 mM, range 0.55–3.61) compared with controls (1.91 mM, range 0.87–3.51; P = .0004), and glutathione depletion correlated with both illness severity ( P = .038) and mortality ( P = .010). Cats had higher ascorbate concentrations when ill (10.65 μM, range 1.13–25.26) compared with controls (3.68 μM, range 0.36–13.57; P = .0009).
Conclusions and Clinical Importance: Clinically ill dogs had decreased erythrocyte glutathione concentrations, which could be a marker of illness severity and prognostic of a poor outcome. Clinically ill cats had an unexpectedly high plasma ascorbate, which could represent a unique species response to oxidative stress.     

铁对患肠炎仔猪生长性能·消化率及肠道微生物的影响

研究了添加硫酸亚铁对DDS诱发肠炎仔猪生长性能、消化率及肠道微生物数量的影响,结果表明:在患有肠炎的断奶仔猪日粮中添加低剂量的铁可以提高仔猪的生产性能和消化率,但对治疗腹泻效果不明显;而高剂量的铁易导致肠道粘膜的氧化损伤,加剧肠炎症状,致使消化率、日增重明显降低,肠道微生物菌群失衡。     

白芍制剂对中性粒细胞相关功能及磷酸二酯酶活性的影响

 【目的】以猪中性粒细胞为靶细胞,研究白芍制剂对其相关功能（呼吸爆发和弹性蛋白酶释放）及磷酸二酯酶活性的影响。【方法】中性粒细胞分离纯化后,以细胞色素C还原法检测中性粒细胞呼吸爆发,以弹性蛋白酶底物的减少反映弹性蛋白酶的释放量,以HPLC检测底物cAMP的变化反映磷酸二酯酶的活性等。【结果】白芍制剂呈剂量依赖性抑制中性粒细胞的呼吸爆发（P＜0.001）,3个不同浓度的抑制率分别为33.15%、45.96%和62.22%;对弹性蛋白酶的释放在低浓度时表现抑制作用（P＜0.05）,抑制率为23.22%,在高浓度时表现促进作用;对中性粒细胞磷酸二酯酶活性具有抑制作用,低、高浓度抑制率分别为13.24%和25.87%（P＜0.01）;HPLC指纹图谱分析表明白芍制剂主要存在5种成分。【结论】白芍制剂对猪中性粒细胞呼吸爆发具有明显的抑制作用,对弹性蛋白酶释放在低浓度有显著抑制作用,其作用机制可能与白芍制剂对磷酸二酯酶活性的抑制有关。     

Effect of germination on total phenolic compounds,total antioxidant capacity,Maillard reaction products and oxidative stress markers in canihua (Chenopodium pallidicaule)

Germination of cereals/pseudo-cereals has been suggested as an effective method to increase antioxidant compounds. However, this process could also lead to high reducing sugar levels and subsequent Maillard reaction products. The aim of this work was to determine the time course effect of canihua (Chenopodium pallidicaule) germination on: 1) antioxidant capacity, 2) extractable and non-extractable phenolic compounds content, 3) Maillard reaction products and 4) oxidative stress markers. Germination increased antioxidant capacity, phenolic compounds and Maillard reaction products, including advanced glycated end products while it decreased oxidative stress markers. All parameters exhibited a similar time course pattern with a maximum at 72 h. In addition to the increase in phenolic compounds and antioxidant capacity, canihua germination produced advanced glycated end products. The impact on human health of these compounds in germinated seeds deserves future attention.     

獐牙菜苦苷对H2O2诱导大鼠心肌细胞凋亡的保护作用

[目的]观察獐牙菜苦苷对氧化应激引起的大鼠心肌细胞凋亡的保护作用,初步探讨獐牙菜苦苷抗心肌细胞氧化应激的保护作用机制。[方法]用差速贴壁法培养SD乳鼠心肌细胞,检测不同给药组中SD乳鼠细胞心肌细胞存活率以及培养液中超氧化物岐化酶（SOD）、丙二醛（MDA）含量;用免疫细胞化学检测心肌细胞的相关凋亡蛋白bcl-2、Bax表达;用吖啶橙荧光染色检测细胞的凋亡情况。[结果]3种不同浓度獐牙菜苦苷均能提高心肌细胞存活率和细胞上清液中SOD含量,且能降低MDA含量,与H2O2刺激组比较有显著性差异（P〈0.05;P〈0.01）。[结论]獐牙菜苦苷对H2O2诱导损伤的心肌细胞有保护作用,其作用机制可能是通过影响氧化系统以及调控特异性蛋白来抑制心肌细胞凋亡。     

狭卵链格孢菌毒素细交链孢菌酮酸诱导稗草叶片氧化胁迫和抗氧化酶变化的研究

[目的]确定细交链孢菌酮酸（tenuazonic acid,TeA）对稗草的毒害作用是否与其诱导氧化胁迫及抗氧化酶活性变化有关。[方法]通过离体试验研究了TeA处理稗草叶片丙二醛和过氧化氢含量及抗氧化酶活性的变化。[结果]稗草叶片经500μmol/L TeA处理后,叶片中丙二醛和过氧化氢含量分别较对照增加了247.86%和67.00%,表明TeA处理诱导了稗草叶片中活性氧暴发,并导致丙二醛和过氧化氢的大量积累。TeA引起超氧化物歧化酶（SOD）、谷胱甘肽还原酶（GR）和过氧化氢酶（CAT）活性显著升高,其中在500μmol/LTeA处理下,稗草叶片SOD、GR和CAT活性均较对照增加1倍以上。[结论]TeA诱导活性氧的产生引起稗草叶片氧化胁迫,同时诱导叶片抗氧化酶活性升高。     

Effect of α tocopherol and selenium on antioxidant status, lipid peroxidation and hepatopathy induced by malathion in chicks

The objective of the present study was to investigate the role of α tocopherol and selenium on malathion induced hepatic damage, and antioxidant defense in chicks. The chicks were divided into three groups. First group received malathion 10 mg/kg BW, orally for 60 days, the second group received the same dose of malathion but was supplemented with α tocopherol and selenium for 60 days and the third group served as the control. A compromised antioxidant capacity as evidenced by increased levels of erythrocytic lipid peroxidation and decreased concentration of vitamin E and decreased activity of glutathione peroxidase was observed in chicks following the administration of malathion. An improved antioxidant status was observed in chicks of second group with α tocopherol and selenium supplementation including higher concentration of vitamin E, increased activity of glutathione peroxidase and lower levels of lipid peroxidation. Histopathological studies of liver in the chicks which received malathion exhibited, moderate to severe degenerative and necrotic changes in the hepatocytes. The correlation of decreased antioxidant status of chicks with degenerative changes in liver suggests that lipid peroxidation may be one of the important mechanism in the chronic toxicity of malathion. The results indicate that α tocopherol and selenium were effective in partially alleviating degenerative changes induced by malathion in the liver of chicks by attenuating processes leading to lipid peroxidation.