A colorimetric method for the determination of serum glutamic oxalacetic and glutamic pyruvic transaminases.
01 Jul 1957-American Journal of Clinical Pathology (AMERICAN JOURNAL OF CLINICAL PATHOLOGY)-Vol. 28, Iss: 1, pp 56-63
About: This article is published in American Journal of Clinical Pathology.The article was published on 1957-07-01. It has received 9424 citations till now.
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TL;DR: It is demonstrated for the first time that SFN is a potentially effective antitumor agent for thyroid cancer.
Abstract: Sulforaphane (SFN), a natural compound derived from broccoli/broccoli sprouts, has been demonstrated to be used as an antitumor agent in different types of cancers. However, its antitumor effect in thyroid cancer remains largely unknown. The aim of the study was to investigate the therapeutic potential of SFN for thyroid cancer and explore the mechanisms underlying antitumor effects of SFN by in vitro and in vivo studies. Our data demonstrated that SFN significantly inhibited thyroid cancer cell proliferation in a dose- and time-dependent manner, induced G2/M phase cell cycle arrest and apoptosis, and inhibited thyroid cancer cell migration and invasion by suppressing epithelial-mesenchymal transition (EMT) process and expression of Slug, Twist, MMP-2 and -9. Mechanically, SFN inhibited thyroid cancer cell growth and invasiveness through repressing phosphorylation of Akt, enhancing p21 expression by the activation of Erk and p38 signaling cascades, and promoting mitochondrial-mediated apoptosis via reactive oxygen species (ROS)-dependent pathway. Growth of xenograft tumors derived from thyroid cancer cell line FTC133 in nude mice was also significantly inhibited by SFN. Importantly, we did not find significant effect of SFN on body weight and liver function of mice. Collectively, we for the first time demonstrate that SFN is a potentially effective antitumor agent for thyroid cancer.
57 citations
TL;DR: TQ administration normalized AA-induced changes in most serum parameters and enhanced the antioxidant capacity in the liver, kidney, and brain tissues in a dose-dependent manner, showing that TQ exerted protective and antioxidant activities againstAA-induced toxicity in mice.
Abstract: Acrylamide (AA), an industrial monomer, may cause multi-organ toxicity through induction of oxidative stress and inflammation. The antioxidant properties of thymoquinone (TQ), an active constituent of Nigella sativa, have been established before. The aim of the current study was to assess the protective effects of TQ against AA-induced toxicity in rats. Forty-eight male Wistar rats were divided into six groups each of eight rats. The first group acted as a negative control and received normal saline. Groups II and III were administered TQ orally at doses of 10 and 20 mg/kg b.wt., respectively, for 21 days. The four group received AA (20 mg/kg b.wt.) for 14 days. The five and six groups were given TQ at either dose for 21 days, starting seven days before AA supplementation (for 14 days). Acrylamide intoxication was associated with significant (p < 0.05) increases in serum levels of liver injury biomarkers (alanine transferase, aspartate transferase, and alkaline phosphatase), renal function products (urea, creatinine), DNA oxidative damage biomarker (8-oxo-2'-deoxyguanosine), and pro-inflammatory biomarkers (interleukin-1β, interleukin-6, and tumor necrosis factor-α). Moreover, AA intoxication was associated with increased lipid peroxidation and nitric oxide levels, while reduced glutathione concentration and activities of glutathione peroxidase, superoxide dismutase, and catalase in the liver, kidney, and brain. TQ administration normalized AA-induced changes in most serum parameters and enhanced the antioxidant capacity in the liver, kidney, and brain tissues in a dose-dependent manner. In conclusion, the current experiment showed that TQ exerted protective and antioxidant activities against AA-induced toxicity in mice.
57 citations
TL;DR: The observations support the idea that IL-22 but not IL-17 provides protection from the potentially lethal effects of liver damage during a primary P. chabaudi infection.
Abstract: The host response following malaria infection depends on a fine balance between levels of pro-inflammatory and anti-inflammatory mediators resulting in the resolution of the infection or immune-mediated pathology. Whilst other components of the innate immune system contribute to the pro-inflammatory milieu, T cells play a major role. For blood-stage malaria, CD4(+) and γδ T cells are major producers of the IFN-γ that controls parasitemia, however, a role for TH17 cells secreting IL-17A and other cytokines, including IL-17F and IL-22 has not yet been investigated in malaria. TH17 cells have been shown to play a role in some protozoan infections, but they also are a source of pro-inflammatory cytokines known to be involved in protection or pathogenicity of infections. In the present study, we have investigated whether IL-17A and IL-22 are induced during a Plasmodium chabaudi infection in mice, and whether these cytokines contribute to either protection or to pathology induced during the infection. Although small numbers of IL-17- and IL-22-producing CD4 T cells are induced in the spleens of infected mice, a more pronounced induction is observed in the liver, where increases in mRNA for IL-17A and, to a lesser extent, IL-22 were observed and CD8(+) T cells, rather than CD4 T cells, are a major source of these cytokines in this organ. Although the lack of IL-17 did not affect the outcome of infection or pathology, lack of IL-22 resulted in 50% mortality within 12 days after infection with significantly greater weight loss at the peak of infection and significant increase in alanine transaminase in the plasma in the acute infection. As parasitemias and temperature were similar in IL-22 KO and wild-type control mice, our observations support the idea that IL-22 but not IL-17 provides protection from the potentially lethal effects of liver damage during a primary P. chabaudi infection.
57 citations
TL;DR: The results show that caffeine prevents experimental cirrhosis; the mechanisms of action are associated with its antioxidant properties and mainly by its ability to block the elevation of the profibrogenic cytokine transforming growth factor-&bgr;, which may be associated with attenuation of the inflammatory and fibrotic processes.
Abstract: BackgroundThere is a growing body of evidence that caffeine exerts beneficial effects on the liver; however, the molecular mechanisms by which caffeine exerts beneficial effects on the liver are poorly defined.AimsThe aim of the present study was to examine the efficacy of caffeine in preventing thi
57 citations
TL;DR: From this study it can be concluded that high fat diet increased arsenic induced oxidative stress.
57 citations