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Hydrocarbon Hydroxylase (hydrocarbon + hydroxylase)

Distribution by Scientific Domains
Medical Sciences100%

Kinds of Hydrocarbon Hydroxylase

  • aryl hydrocarbon hydroxylase
    		•

    Selected Abstracts

    Inhibitory effect of apigenin on benzo(a)pyrene-mediated genotoxicity in Swiss albino mice

    JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 12 2006
    Tajdar Husain Khan
    Apigenin, a bioflavonoid, is abundantly present in fruits and vegetables and possesses potential chemopreventive properties against a wide variety of chronic diseases. In this study we investigated the anti-genotoxic effects of apigenin against a known genotoxicant, benzo(a)pyrene (B(a)P) (125 mg kg,1 orally) toxicity in Swiss albino mice. B(a)P administration led to induction of cytochrome P-450 (CYP), aryl hydrocarbon hydroxylase (AHH) and DNA strand breaks (P < 0.001), which was suppressed by apigenin (2.5 and 5 mg kg,1 orally) dose dependently (P < 0.001). B(a)P-induced depletion in the level of reduced glutathione (GSH), quinone reductase (QR) and glutathione-S-transferase (GST) was also shown to be restored by apigenin pre-treatment (P < 0.001). A simultaneous significant and dose-dependent reduction was noted in DNA strand breaks and in-vivo DNA damage (P < 0.001), which gives some insight into restoration of DNA integrity in modulator groups. These results strongly support the protective nature of apigenin against B(a)P-induced toxicity. [source]

    Assessment of carcinogenic potential of repeated fish fried oil in mice

    MOLECULAR CARCINOGENESIS, Issue 10 2006
    Manoj K. Pandey
    Abstract Our prior studies have shown that single topical treatment of repeated fish fried oil extract (RFFE), containing various polycyclic aromatic hydrocarbons (PAHs), to the dorsal epidermis of mice caused enhancement of DNA damage along with higher expression of p53 and p21WAF1 proteins and cell-cycle arrest. In the present study carcinogenic potential of repeated fish fried oil (RFFO) and RFFE was assessed. Single topical application of RFFO (100 µL/animal) and RFFE (100,500 µg/animal) to Swiss albino female mice resulted in significant induction (1.8- to 7.4-fold) of ornithine decarboxylase activity. Twice weekly topical application of methylcholanthrene (MCA) for 24 wk or single topical application of 7,12-dimethylbenzanthracene (DMBA) or RFFO or RFFE, as initiator followed by twice weekly application of 12-O-tetradecanoyl phorbol myristate acetate (TPA) as promoter for 24 wk, resulted in development of skin papillomas after 6, 7, 18, and 9 wk, respectively. The cumulative number of tumors in MCA, DMBA/TPA, RFFE (200 µg)/TPA, and RFFE (500 µg)/TPA groups were 276, 168, 34, and 58 after 24 wk while negligible or minimal initiating activity was noticed in RFFO/TPA group. No tumors were found in animals either given twice weekly topical application of RFFO or a single initiating dose of DMBA followed by twice weekly application of RFFO. Histopathology of skin of animals treated with RFFE/TPA showed marked proliferation of epidermal layers along with abnormal mitosis and multinucleated tumor appearance. Skin of animals in groups RFFO/TPA and DMBA/RFFO showed sloughing and regeneration of epidermal layers, oedema along with proliferation of fibroblasts. Histochemical localization of ,-glutamyl transpeptidase was found to be substantially higher in skin of mice treated with RFFO/TPA and RFFE/TPA. Animals treated with RFFO/TPA, DMBA/RFFO, and RFFE/TPA resulted in significant induction of cutaneous aryl hydrocarbon hydroxylase (AHH) (421,432%), ethoxyresorufin-O-deethylase (252,316%), and glutathione S-transferase (133,245%) activities. Animals treated with RFFO/TPA, DMBA/RFFO, and RFFE/TPA led to significant reduction in glutathione content (39,44%) with a concomitant increase in lipid peroxidation (254,492%). Animals treated with RFFO/TPA and RFFE/TPA led a significant decrease in catalase (43,69%) and superoxide dismutase (20,31%) activities while glutathione reductase activity was found to be diminished (23,51%) in RFFO, RFFO/TPA, DMBA/RFFO, and RFFE/TPA treated groups. These results suggest that RFFE possess skin tumor initiating activity and that it may have weak promoting activity as well, which may involve free radicals. © 2006 Wiley-Liss, Inc. [source]

    Azadirachta indica modulates carcinogen biotransformation and reduced glutathione at peri-initiation phase of benzo(a)pyrene induced murine forestomach tumorigenesis

    PHYTOTHERAPY RESEARCH, Issue 9 2008
    Subhash Chander Gangar
    Abstract The present study evaluated the effects of aqueous Azadirachta indica leaf extract (AAILE) on the activities of certain phase I (cytochrome P450, cytochrome b5 and aryl hydrocarbon hydroxylase) as well as phase II (glutathione- S -transferase and UDP-glucuronosyl transferase) biotransformation enzymes; and reduced glutathione (GSH) (in forestomach and hepatic tissues) during/after intra-gastric instillations of B(a)P in murine forestomach tumorigenesis bioassay protocol. The activities of phase I biotransformation enzymes were found to increase, whereas a decrease in GSH content as well as glutathione- S -transferase was observed in mice receiving only B(a)P during as well as 2 weeks after B(a)P instillations. The activity of UDP-glucuronosyltransferase decreased during B(a)P instillations, whereas after the latter, the activity increased when compared with the control mice. However, in mice that received AAILE along with B(a)P instillations, a decrease in phase I enzymes was accompanied by an increase in phase II enzymes as well as GSH contents. Only AAILE treatment reduced the activities of phase I biotransformation enzymes and enhanced the GSH contents as well as the activities of phase II enzymes. Observations of the present study seem to be quite significant and (when taken together with our earlier findings) provides evidence for A. indica mediated modulation of the peri-initiation phase of the process of forestomach tumorigenesis. Copyright © 2008 John Wiley & Sons, Ltd. [source]

    Chemopreventive Task of Capsaicin against Benzo(a)pyrene-induced Lung Cancer in Swiss Albino Mice

    BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 5 2009
    Pandi Anandakumar
    The present study is an effort to identify the chemopreventive role of alkaloid capsaicin against benzo(a)pyrene-induced lung cancer in Swiss albino mice. Benzo(a)pyrene-induced lung cancer-bearing animals showed abnormal changes in body weight, lung weight, tumour incidence and alterations in the activities of marker enzymes adenosine deaminase, aryl hydrocarbon hydroxylase, ,-glutamyl transpeptidase, 5,-nucleotidase and lactate dehydrogenase. On capsaicin pre-co-treatment, all the above alterations were returned to near normal. Immunohistochemical analysis of proliferating cell nuclear antigen together with lung histological examination further supported our biochemical findings that demonstrated the chemoprotective role of capsaicin against benzo(a)pyrene-induced experimental lung cancer. [source]