Effects of diazinon at different doses on rat liver and pancreas tissues

Diazinon is one of the most widely used organophosphates in agriculture. Toxic effects of diazinon are due to the inhibition of acetylcholinesterase, an enzyme needed for proper nervous system function. This study was designed to investigate the effects of diazinon at different doses on pancreas and liver tissues and in which dose level diazinon shows its effects. Sixty male Wistar albino rats were included in this study. Animals were initially divided into control and diazinon given groups. There were 10 animals in the control group and 50 animals in diazinon administered group. The latter was divided into five equal subgroups: 25, 50, 100, 200 and 300 mg/kg of diazinon administered groups. Control group was given only saline. All animals in 300 mg/kg diazinon group died. After 24 h, rats were sacrificed under ether anesthesia. Tissue and blood samples were taken for biochemical and histopathological analysis. Sample tissues were examined under light microscope. In biochemical analysis, AST, ALT, LDH, amylase and lipase enzyme activities were measured. One-way ANOVA test was used to compare the groups. In 200 mg/kg diazinon given group, it has been observed some histopathological changes in pancreas and liver tissues. Cholinesterase activities were significantly decreased and alkaline phosphatase levels were increased in all diazinon given groups, when compared with the controls. There was statistically significant difference between the control and diazinon given groups by means of serum amylase, lipase, ALT and AST activities (p < 0.05). LDH activities were significantly increased in 100 and 200 mg diazinon given groups, when compared with the controls (p < 0.05). Histopathological changes were observed only in 200 mg diazinon given group. This evidence suggest that diazinon effect is dose dependent and this is possibly 10-15% of the LD₅₀ dose (200 mg/kg), which cause acute pancreatitis and histopathological changes in liver.     

Effects of angiotensin II and losartan on collagen synthesis in rat hepatic stellate cells

AIM: To investigate the effects of angiotensin II (Ang II) and AT_1a receptor antagonist (losartan) collagen synthesis in rat hepatic stellate cells (HSCs). METHODS: ① Rat HSCs were isolated, cultured and identified. ② Rat HSCs were incubated in the medium with different concentrations of AngII or losartan, then the quantity of collagen was examined by -proline release assay. RESULTS: ① The yield of HSCs was 2×10⁷-3×10⁷/per rat, their viability and purity was more than 95% and 90%, respectively. ② The yield of collagen in HSCs significantly got a rise in a concentration-dependent manner when HSCs were incubated with AngII (10^－6mol/L-10^－10 mol/L) (P<0.05). While HSCs were influenced by the antagonist of AT_1a (10^－6 mol/L-10^－9 mol/L), the quantity of collagen dropped greatly (P<0.05). CONCLUSIONS: Ang II stimulates HSCs to produce more collagen. Losartan inhibits the cell to synthesize collagen via AT_1a receptor (P<0.05). The results indicate that Ang II may play an important role in the development of hepatic fibrosis, and using AT_1a antagonist may offer a new strategy to prevent hepatic fibrosis.     

Effects of c-myb antisense RNA on the proliferation and collagen Ⅰ gene expression in cultured hepatic stellate cells

AIM:To investigate the effects of c-myb antisense RNA on the proriferation and collagen Ⅰ gene expression in cultured hepatic stellate cells(HSC) in rats.METHODS:The c-myb antisense gene recombinant retroviral vector(pDOR-myb) was constructed, and then was transfected into retroviral package cell line PA 317 by means of N-[1-(2,3-Dioleoyloxy) propyl]-N, N, N-trimethylammonium methyl-sulfate(DOTAP) liposomal transfection reagent. The pseudoviruses produced from the resistant PA317 cells selected with G418 were collected, with which HSCs isolated from rat liver were infected. The cell proliferation was measured by MTT method, c-myb, α₁-Ⅰ collagen mRNA expression and c-myb protein in HSCs were detected with semi-quantitative RT-PCR and western-blot, respectively.RESULTS:HSCs from rats were isolated successfully with the viability >98%. In the pDOR-myb infected HSCs, c-myb expression levels, the cell proliferation, and α₁-Ⅰ collagen mRNA expression were repressed significantly.CONCLUSIONS:c-myb plays a key role in the activation and proliferation of HSC. c-myb antisense RNA can inhibit cell proliferation and α₁-Ⅰ collagen mRNA expression in the infected HSC. These data suggest that inhibition of c-myb gene expression would be a potential way for the treatment of liver fibrosis.     

IMAGING DIAGNOSIS—ULTRASONOGRAPHIC AND CT FINDINGS IN A GRAY SEAL (HALICHOERUS GRYPUS) WITH HEPATIC CIRRHOSIS,PYELONEPHRITIS, AND NEPHROLITHIASIS

An immature gray seal was presented with lethargy, weight loss, vomiting and hematuria. Hepatic disease and urinary tract infection were suspected. Abdominal ultrasound showed hyperechoic structures with marked acoustic shadowing spread throughout both kidneys, but incomplete visualization of the liver. Abdominal CT showed mineral densities scattered throughout both kidneys and poor delineation of the liver. Due to the poor quality of life, the seal was euthanized. Postmortem examination showed ammonium urate nephroliths, pyelonephritis, and hepatic cirrhosis. This case report emphasizes the difficulty of characterizing liver disease with conventional 2D‐ultrasound and CT in a deep‐chested animal with minimal intra‐abdominal fat.     

In ovo leptin administration affects hepatic lipid metabolism and microRNA expression in newly hatched broiler chickens

Background: A leptin-like immunoreactive substance has been found in chicken eggs and has been implicated in serving as a maternal signal to program offspring growth and metabolism. In the present study, we investigated the effects of in ovo leptin administration on hatch weight, serum and hepatic concentrations of metabolites and hormones, as well as on the expression of genes involved in hepatic lipid metabolism and the predicted microRNAs (miRNAs) targeting the affected genes. To this end we injected fertile eggs with either 0.5 μg of recombinant murine leptin or vehicle (PBS) before incubation. Results: Prenatally leptin-exposed chicks showed lower hatch weight, but higher liver weight relative to the body weight, compared to the control group. In ovo leptin treatment increased the hepatic content and serum concentration of leptin in newly hatched chickens. The hepatic contents of triglycerides (TG) and total cholesterol (Tch) were decreased, whereas the serum levels of TG, Tch and apolipoprotein B (ApoB) were increased. The hepatic mRNA expression of sterol regulator element binding protein 1 (SREBP-1c), SREBP-2, hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) and cholesterol 7α-hydroxylase 1 (CYP7A1) was significantly up-regulated, as was the protein content of both SREBP-1c and SREBP-2 in hepatic nuclear extracts of leptin-treated chickens. Moreover, out of 12 miRNAs targeting SREBP-1c and/or HMGCR, five were significantly up-regulated in liver of leptin-treated chicks, including gga-miR-200b and gga-miR-429, which target both SREBP-1c and HMGCR. Conclusions: These results suggest that leptin in ovo decreases hatch weight, and modifies hepatic leptin secretion and lipid metabolism in newly hatched broiler chickens, possibly via microRNA-mediated gene regulation.     

Estradiol-17β and linseed meal interact to alter visceral organ mass and hormone concentrations from ovariectomized ewes

To evaluate the estrogenic potential of secoisolariciresinol diglycoside (SDG) found in linseed meal (LSM) on visceral organ mass, IGF-I, and thyroid hormone (T₃ and T₄) concentrations, 48 multiparous, ovariectomized ewes (54.6 ± 1.1 kg) were used in a 3 × 4 factorial arrangement. Main effects were length of LSM feeding (0, 1, 7, or 14 d) and length of exposure to estradiol-17β (E₂) implant (0, 6, or 24 h prior to tissue collection). Implanting ewes with E₂ for 24 h increased liver mass relative to empty body weight (EBW; g/kg EBW) compared with ewes implanted for 0 or 6 h (P ≤ 0.03), whereas feeding LSM for 14 d decreased liver mass compared with ewes fed LSM for 1 or 7 d (P ≤ 0.02). There was an LSM × E₂ interaction (P = 0.01) for duodenal mass (g/kg EBW), LSM, and E₂ tended (P = 0.07) to influence the stomach complex mass; however, ileal mass was not affected. Neither LSM nor E₂ affected (P ≥ 0.12) CYP2C or CYP3A mRNA expression or cellularity of the liver. Exogenous E₂ influenced circulating concentrations of IGF-I, T₃, and T₄. The estrogenic or anti-estrogenic potential of LSM is dependent upon the tissue, exposure to E₂, and the duration of LSM feeding. Feeding LSM during gestation, lactation, or during the grow-finish phase warrants further investigation.     

Recent advances in nm-23 gene and hepatocellular carcinoma

nm-23 gene is the first antimetastatic gene which was found to have close relationship with metastasis and prognosis of many malignant carcinoma. This review briefly summarizes the development of nm-23 gene and hepatocellular carcinoma in recent years.     

鹅终止填饲后肝脏的生理性恢复试验

鹅短期强制填饲形成肥肝后,终止填饲观察肝脏生理性恢复情况。终填15 d、30 d后,体重和肝脏重快速恢复,接近正常;血液中TBA、TG等变化规律不明显,CHO终填30 d恢复,TP、ALB、GLO等体症蛋白含量变化不显著,ALT、AST、LDH、CHE等酶类填饲后大幅上升,终填后迅速回复,其中AST填后含量达191.8 U.L-1,升高2.87倍,终填15 d、30 d回复到正常的106.67%和84.44%;肝细胞内脂肪空泡迅速减少,终填30 d基本消失,向正常肝细胞过渡。试验结果表明肥肝生产是正常可逆的生理过程,通过自然放养,可基本回复到正常状态。