Abstract

The present study was undertaken to evaluate the possible ameliorative role of grape seed proanthocyanidins (GSP) against Cadmium (Cd) induced hepatic inflammation, apoptosis and hepatic mitochondrial toxicity in rats. Male Wistar rats were distributed in four experimental groups: control, GSP, Cd and Cd + GSP. Exposure to a hepatotoxic dose of Cd (5 mg/kg BW) caused liver damage, coupled with enhanced reactive oxygen species (ROS) generation, increased inflammation and apoptosis in liver with increased DNA damage in hepatocytes of rats. Mitochondria were isolated from the hepatic tissues of rats from each group. Our results showed significant decrease in the tri-carboxylic acid cycle enzymes, increased mitochondrial swelling, inhibition of cytochrome c oxidase activity and complex I–III, II–III and IV mediated electron transfer, decreased mitochondrial ATPases, a reduction in calcium content and mitochondrial oxygen consumption in Cd treated rats. All these molecular changes caused by Cd were alleviated by the pre-supplementation with GSP (100 mg/kg BW). The ultra structural changes in the liver also support our findings. From our results, it is clearly indicated that the free radical scavenging, metal chelating and antioxidant potentials of GSP might be the possible reason, responsible for the rescue action against Cd induced mitochondrial damage in the liver of rats.

Abstract

Taiwan implemented a comprehensive and universal National Health Insurance (NHI) program to cover all inhabitants. This study aimed to assess the medical utilization by liver cancer patients under the NHI. This retrospective cross-sectional study used a sampled NHI research database, which contained 1 million beneficiaries. The claims of liver cancer patients in 2009 were analyzed. The other beneficiaries without liver cancer who used medical services in 2009 served as the control patients. Among the 2335 identified liver cancer patients, 2178 (93.3%) patients used outpatient services and 1193 (51.1%) patients used inpatient services. Liver cancer accounted for 1.8% of the NHI’s total cost. The cost per visit was United States dollars (US$)59.30 for outpatient care and US$2070.30 for inpatient care. The annual cost per patient was US$4746.60, US$1951.00 were for outpatient care and US$2795.60 for inpatient care. Patients who were female, in their 60s, had a lower income, and lived in southern Taiwan had a higher cost per patient (p < 0.0001). Fees for consultation, treatment, and medical supplies (57.3%) accounted for the highest portion of outpatient costs, followed by drug fees (30.0%) and diagnosis fees (11.2%). Ward fees accounted for the highest portion of inpatient costs (19.0%), followed by drug fees (18.7%) and X-ray fees (14.9%). Private hospitals were visited more frequently than public hospitals. The cost per visit and cost per patient with liver cancer were 206.0% and 666.8%, respectively, of the cost of the control patients. The cost of liver cancer care is substantial and varies by sex, age, income, and geographic distribution. It is critical to reduce the incidence of liver cancer and identify cost-effective treatment strategies.

Abstract

Perivascular epithelioid cell tumor (PEComa) is a rare tumor. Here, we present data regarding clinical presentations, diagnoses, management, and prognosis of five cases of hepatic PEComa between January 2002 and December 2008. Ultrasonography showed hyperechoic masses in all patients. Precontrast computed tomography (CT) showed that all lesions scanned were heterogeneous in density and were heterogeneously enhanced in arterial phase images. In two cases, magnetic resonance imaging showed hypointensity on T1-weighted images and hyperintensity on T2-weighted images. In enhanced scanning, lesions showed asymmetrical enhancement during arterial phase imaging. All tumors were composed of varying proportions of smooth muscle, adipose tissue, and thick-walled blood vessels, and showed positive immunohistochemical staining for Human Melanoma Black-45. All patients underwent hepatectomy, and there was no evidence of recurrence or metastasis during the follow-up period.

Abstract

We report a case of pseudolymphoma of the liver in a 49-year-old woman without an underlying disease except for liver hemangioma. A 20-mm nodule was incidentally found in segment 2 of the liver by abdominal ultrasonography during a regular follow-up of the hepatic hemangioma. After a series of radiological examinations, a left lateral sectionectomy was performed because malignant hepatic tumor could not be excluded. The patient was discharged uneventfully 7 days after the operation. The pathology examination revealed a pseudolymphoma. No recurrence of the tumor was found 5½ years after the operation. To the best of our knowledge, only 46 cases of pseudolymphoma of the liver have been reported to date. A review of the literature showed that pseudolymphomas occur predominantly in females (89.4%), usually occur as a single tumor (80.4%), are no more than 20 mm in size (90.6%), and are frequently associated with either autoimmune disease or chronic liver disease. Because an accurate diagnosis is difficult to establish, vigilant follow-up is indicated, and surgical intervention is the choice of treatment once the suspiciousness of malignancy has been raised.

Abstract

This study was designed to evaluate the hepatoprotective activity of aqueous extract and isolated flavone (5-hydroxy, 7, 8, 2’trimethoxy flavone) compound of Andrographis alata against CCl4 induced hepatotoxicity. The hepatotoxicity was induced in albino rats CCl4 (i.p.). Analysis of serum ALT, AST and alkaline phosphatase activities with the concentrations of albumin, total protein and bilirubin was carried out. The activities of all the marker enzymes reported a significant elevation in CCl4 treated rats, which were significantly recovered towards an almost normal level in animals simultaneously administered with aqueous extract and flavone compound. This work suggests that aqueous extract and isolated flavone compound of A. alata exert significant therapeutic effect on CCl4 induced hepatotoxicity in rats.

Abstract

Tetrabromobisphenol A (TBBPA), a nongenotoxic flame retardant, causes uterine tumors in female rats. A proposed mode of action (MoA) for these tumors involves an increase in the bioavailability of estradiol as a result of TBBPA inhibiting estrogen sulfotransferases (ES), the enzymes responsible for inactivating and enhancing the elimination of estradiol. The objective of this study was to evaluate the effect of dose and repeated administration of TBBPA on the level of TBBPA, TBBPA-glucuronide (GA) and TBBPA-sulfate (S) conjugates in plasma, liver and uterus of female Wistar Han rats administered TBBPA (50, 100, 250, 500 or 1000 mg/kg) for 28 consecutive days. In accordance with this objective, TBBPA sulfation was used as a surrogate for evaluating the potential for estradiol sulfation to be limited at high dose levels of TBBPA. Blood samples were collected at 4 and 8 h post-dosing on study day 7, 14, and 28, while liver and uterus were collected at the same time points following 28 days of dosing. Tissue samples were analyzed for TBBPA, TBBPA-GA and TBBPA-S by LC–MS/MS. A dose-related increase in the concentration of all three analytes occurred in plasma (day 7, 14, and 28) as well as liver and uterus tissue (day 28) at both 4 and 8 h post dose. The plasma concentration of TBBPA-GA and TBBPA-S was higher in animals dosed for 28 days compared to those dosed for 7 or 14 days showing an increase in systemic circulation of these conjugates with repeated administration. The balance of these conjugates was also different in tissues with TBBPA-S > TBBPA-GA at high doses in the liver and TBBPA-GA > TBBPA-S in both plasma and uterus. In all three tissues the ratio of TBBPA-S/TBBPA-GA showed a decreasing trend with dose, suggesting that at high TBBPA dose levels sulfation of TBBPA becomes limited. This effect was most apparent in the liver and plasma at 28 days of administration. Together these data show that administration of high doses of TBBPA associated with the induction of uterine tumors, results in a disruption in the balance of conjugates reflected by a decrease in the TBBPA-S/TBBPA-GA ratio. A limitation in the sulfation of TBBPA in vivo supports in vitro data defining TBBPA as an inhibitor of ES activity, thus providing further support that the proposed MoA occurs under conditions of high dose, chronic TBBPA administration to Wistar Han rats. Given that the uterine tumors observed in rats (250–1000 mg/kg-day) only occur at very high doses that perturb homeostatic control, it is unlikely such effects would occur in humans given that current TBBPA exposure levels are approximately eight orders of magnitude lower than these doses that are associated with exceeding the capacity of conjugation pathways in animal studies.