Catalase activity in human hepatocellular carcinoma (HCC)

Liver catalase activity, one of the free-radical scavenger enzymes, has been measured in 22 normal subjects and compared with that of 13 patients suffering from hepatocellular carcinoma. The activity was estimated both in tumor tissue and in tumor-free tissue. A significant reduction of catalase activity was noted in tumor tissue (p < 0.001) as well as in the adjacent tumor-free tissue (p < 0.02). In patients with hepatoma, the serum iron level was lower than in normal (p < 0.01) and was correlated with enzyme activity (r = 0.958). These findings suggest that in hepatocarcinoma the free radical scavenger system is impaired.     

钼酸铵显色法测定血清过氧化氢酶

介绍一种简便的以钼酸铵显色的血清过氧化氢酶分光光度测定法。该法酶活性在１００ｋＵ／Ｌ内呈良好线性。批内变异ＣＶ＝３．６％，天间变异ＣＶ＝４．５７％。平均回收率为１００．１４％。高ＴＧ、高Ｂｉｌ血清标本，可使Ａ值增加，但不影响Ｃａｔ测定值。ＶｉｔＣ、肝素均可使酶活性减低。由于红细胞内富含Ｃａｔ，溶血标本能显著增加酶活性。血清标本酶活性在－４℃４８ｈ内无变化，在－２５℃能保持５～６周。３８８例体检健康者血清Ｃａｔｘ＝５７．６１ＫＵ／Ｌ，经Ｄ检验，当Ｐ＝０．０５时，属正态分布；Ｐ＝０．１时，属非正态分布。中位数（Ｍｄ）＝５６．２２ＫＵ／Ｌ，百分位数法计算，其９５％范围为２１．５８～１０８．８７（ｋＵ／Ｌ）。初步观察１１９例患者Ｃａｔ活性，显示各类癌症患者Ｃａｔ活性明显减低。     

阿司匹林联合奥扎格雷钠对急性脑梗死患者血清hs-CRP、FIB、MDA、SOD及CAT表达水平的影响

目的观察阿司匹林联合奥扎格雷钠对急性脑梗死患者血清超敏C反应蛋白(hs-CRP)、纤维蛋白原(FIB)、丙二醛(MDA)、超氧化物歧化酶(SOD)及过氧化氢酶(CAT)表达水平的影响。方法将脑梗死急性发作患者107例随机分为对照组54例和观察组53例,对照组给予阿司匹林,观察组给予阿司匹林联合奥扎格雷钠。对比2组治疗前后血清hs-CRP、FIB、MDA、SOD和CAT表达水平,运用美国国立卫生研究院卒中量表(NIHSS)评分和日常生活能力表Barthel指数(BI)评估2组神经功能缺损程度改善情况。结果治疗后14 d,2组hs-CRP、FIB和MDA水平下降,SOD和CAT水平较治疗前上升(P0.05或P0.01),且观察组hs-CRP、FIB和MDA水平显著低于对照组(P0.01),SOD、CAT水平显著高于对照组(P0.05)。治疗后1个月,2组NHISS评分较治疗前下降(P0.05),BI指数较治疗前上升(P0.05),且观察组改善显著优于对照组(P0.05)。结论阿司匹林联合奥扎格雷钠能有效改善急性脑梗死患者氧自由基和抗氧化系统间平衡,减轻脑细胞损伤,恢复受损的神经功能。     

Neuroprotective effect of ginger on anti-oxidant enzymes in streptozotocin-induced diabetic rats

The aim of the present study was to investigate the effect of ginger on oxidative stress markers in the mitochondrial fractions of cerebral cortex (CC), cerebellum (CB), hippocampus (HC) and hypothalamus (HT) of diabetic rats. Diabetes exacerbates neuronal injury induced by hyperglycemia mediated oxidative damage. A marked decrease in anti-oxidant marker enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), reduced glutathione (GSH) and increase in malondialdehyde (MDA) was observed in the diabetic rats. Decreased activities of anti-oxidant enzymes in diabetic rats were augmented on oral administration of ginger. Moreover, ginger administration depleted the MDA level, which was earlier increased in the diabetic rats. These results suggest that ginger exhibit a neuroprotective effect by accelerating brain anti-oxidant defense mechanisms and down regulating the MDA levels to the normal levels in the diabetic rats. Thus, ginger may be used as therapeutic agent in preventing complications in diabetic patients.     

Protective effect of gallic acid against lindane induced toxicity in experimental rats

Lindane is an organochlorine pesticide that persists in the environment, bioaccumulate through food chain and has a risk of causing adverse effects to human health and the environment. It induces cell damage by producing free radicals and reactive oxygen species. The aim of the present study is to investigate the protective effect of gallic acid (a plant derived polyphenol) against lindane induced hepatic and renal toxicity in rats. Liver damage was assessed by hepatic serum marker enzymes like SGOT, SGPT and ALP and histopathological observation. Renal damage was observed by histopathological examination and serum markers like creatinine and urea. Treatment with lindane increased the levels of lipid peroxidation, serum marker enzyme activity with a concomitant decrease in GSH, CAT, SOD, GPx and GST. Histological alterations were also observed in kidney and liver tissue with lindane treatment. Co-treatment of gallic acid significantly prevented the lindane induced alterations in kidney and liver tissues with a decrease in LPO, serum marker enzyme activity and a significant increase in antioxidant levels. These results suggest that gallic acid has protective effect over lindane induced oxidative damage in rat liver and kidney.     

Antihyperglycemic and antioxidative potential of Psidium guajava fruit in streptozotocin-induced diabetic rats

Psidium guajava Linn. (family Myrtaceae; PG) is a tropical fruit with a blood-glucose-lowering effect in diabetic rats, but its mechanism of action is still unknown. We investigated the antihyperglycemic efficacy and mechanisms of action of PG in streptozotocin (STZ)-induced diabetic rats. After 4 weeks of PG supplementation (125 and 250 mg/kg), PG significantly restored the loss of body weight caused by STZ and reduced blood glucose levels in a dose-dependent manner compared with that in diabetic control rats. Mechanistically, PG protected pancreatic tissues, including islet β-cells, against lipid peroxidation and DNA strand breaks induced by STZ, and thus reduced the loss of insulin-positive β-cells and insulin secretion. Moreover, PG also markedly inhibited pancreatic nuclear factor-kappa B protein expression induced by STZ and restored the activities of antioxidant enzymes, including superoxide dismutase, catalase, and glutathione peroxidase. We conclude that PG has a significant antihyperglycemic effect, and that this effect is associated with its antioxidative activity.     

Protective role of puerarin on lead-induced alterations of the hepatic glutathione antioxidant system and hyperlipidemia in rats

Puerarin (PU), a natural flavonoid, has been reported to have many benefits and medicinal properties. The aim of the present study was to investigate the effects of puerarin on hepatic oxidative stress and hyperlipidemia in rats exposed to lead. Our data showed that puerarin significantly prevented lead-induced hepatotoxicity, indicated by both diagnostic indicators of liver damage (serum aminotransferase levels) and histopathological analysis. Moreover, lead-induced profound elevation of ROS production and oxidative stress, as evidenced by increasing of lipid peroxidation level, reducing of GPx, GST, GR and GCL activities and depleting of intracellular reduced GSH level in liver, were suppressed by treatment with puerarin. Furthermore, the increase of serum cholesterol, triglycerides and LDL induced by lead was effectively suppressed by puerarin. The HDL level in the lead treatment rats was also increased by puerarin. Western blot analysis showed that puerarin remarkably inhibited hyperlipidemia by regulating the expression of cholesterol 7a-hydroxylase (CYP7A1), 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) and low-density lipoprotein receptor (LDL-R) in liver of lead treated rats. Altogether, these results suggest that puerarin could protect the lead-induced liver injury and hyperlipidemia by reducing ROS production, renewing the activities of antioxidant enzymes and influencing expression of hepatic lipid biosynthesis and metabolism genes.     

青枯菌诱导广藿香防御相关酶同工酶分析

目的 研究青枯菌诱导广藿香的致病过程及防御相关酶同工酶的动态变化。方法 利用青枯菌粗毒素诱导广藿香试管苗,并用聚丙烯酰胺凝胶电泳法,对诱导植株中超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、过氧化物酶（POD）同工酶谱带的变化进行分析。结果 青枯菌诱导1～7 d后的广藿香植株,表现渐进的发病过程,开始时,植株失绿、少数叶片萎垂;逐渐植株茎杆弯曲、整株叶片萎蔫。同工酶电泳分析表明,SOD同工酶在第1、3天时分别出现了新谱带,与对照共有的谱带,强度先增后减;CAT同工酶在第3、5天时分别出现新谱带,第6天时强度达到最大;POD同工酶在第1、4天时分别出现了新谱带,强度先增后减,第7天时所有谱带消失。结论 青枯病的发生呈现渐进的过程。青枯菌诱导1～7 d,广藿香SOD、CAT和POD同工酶谱带在数目和强度上均有所不同,呈动态变化,表明SOD、CAT和POD在广藿香抵抗青枯菌入侵时可能起到较为重要的作用。     

l-Theanine prevents alcoholic liver injury through enhancing the antioxidant capability of hepatocytes

l-Theanine is a unique amino acid in green tea. We here evaluated the protective effects of l-theanine on ethanol-induced liver injury in vitro and in vivo. Our results revealed that l-theanine significantly protected hepatocytes against ethanol-induced cell cytotoxicity which displayed by decrease of viability and increase of LDH and AST. Furthermore, the experiments of DAPI staining, pro-caspase3 level and PARP cleavage determination indicated that l-theanine inhibited ethanol-induced L02 cell apoptosis. Mechanically, l-theanine inhibited loss of mitochondrial membrane potential and prevented cytochrome c release from mitochondria in ethanol-treated L02 cells. l-Theanine also prevented ethanol-triggered ROS and MDA generation in L02 cells. l-Theanine restored the antioxidant capability of hepatocytes including GSH content and SOD activity which were reduced by ethanol. In vivo experiments showed that l-theanine significantly inhibited ethanol-stimulated the increase of ALT, AST, TG and MDA in mice. Histopathological examination demonstrated that l-theanine pretreated to mice apparently diminished ethanol-induced fat droplets. In accordance with the in vitro study, l-theanine significantly inhibited ethanol-induced reduction of mouse antioxidant capability which included the activities of SOD, CAT and GR, and level of GSH. These results indicated that l-theanine prevented ethanol-induced liver injury through enhancing hepatocyte antioxidant abilities.