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  • 1
    Online Resource
    Online Resource
    The molecular effect of 1,4,7‐triazacyclononane on oxidative stress parameters in human hepatocellular carcinoma (HepG2) cells
    Wiley ; 2020
    In:  Journal of Biochemical and Molecular Toxicology Vol. 34, No. 12 ( 2020-12)
    Details
    In: Journal of Biochemical and Molecular Toxicology, Wiley, Vol. 34, No. 12 ( 2020-12)
    Abstract: Antibiotic resistance poses a great threat to human, animal and environmental health. β‐Lactam antibiotics have been successful in combating bacterial infections. However, the overuse, inappropriate prescribing, unavailability of new antibiotics and regulation barriers have exacerbated bacterial resistance to these antibiotics. 1,4,7‐Triazacyclononane (TACN) is a cyclic organic tridentate inhibitor with strong metal‐chelating abilities that has been shown to inhibit β‐lactamase enzymes and may represent an important breakthrough in the treatment of drug‐resistant bacterial strains. However, its cytotoxicity in the liver is unknown. This study aimed to determine the effect of TACN on oxidative stress in HepG2 cells. The HepG2 cells were treated with 0 to 500 µM TACN for 24 hours to obtain an IC 50 for use in subsequent assays. Free radicals were measured using the thiobarbituric acid reactive substance and nitric oxide synthase assays, respectively, while antioxidant levels were assessed using luminometry (glutathione [GSH] and adenosine triphosphate [ATP] ) and Western blot analysis (SOD, catalase, GPx‐1, HSP70 and Nrf2). Percentage survival fluctuated as TACN concentration increased with a calculated IC 50 of 545 µM. A slight increase in HSP70 and Nrf2 expression indicated the presence of stress and a response against it, respectively. However, free radical production was not increased as indicated by decreased malondialdehyde levels and reactive nitrogen species. Glutathione levels increased slightly, while ATP levels were marginally altered. The results suggest that TACN does not induce oxidative stress in HepG2 cells and can be exploited as a potential inhibitor.
    Type of Medium: Online Resource
    ISSN: 1095-6670 , 1099-0461
    URL: Issue
    URL: Article
    DOI: 10.1002/jbt.v34.12
    DOI: 10.1002/jbt.22607
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 1481995-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Di‐2‐picolylamine triggers caspase‐independent apoptosis by inducing oxidative stress in human liver hepatocellular carcinoma cells
    Wiley ; 2021
    In:  Biotechnology and Applied Biochemistry Vol. 68, No. 2 ( 2021-04), p. 257-266
    Details
    In: Biotechnology and Applied Biochemistry, Wiley, Vol. 68, No. 2 ( 2021-04), p. 257-266
    Abstract: Di‐2‐picolylamine (DPA) is an organic compound that has been shown to possess antioxidant properties when conjugated to form a metal complex. The basis of this study was to determine the effects of DPA on the proliferation and apoptosis of human hepatocellular carcinoma cells and elucidate the possible mechanisms. The methylthiazol tetrazolium assay served to measure cell viability and generated an IC 50 of 1591 µM. Luminometry was used to investigate caspase activity and ATP concentration. It was observed that the decreased cell viability was associated with reduced ATP levels. Despite increased Bax and caspase 9 activity, cell death was caspase independent as indicated by the reduction in caspase 3/7 activity. This was associated with the downregulation poly(ADP‐ribose) polymerase cleavage (Western blotting). However, the Hoescht assay depicted nuclear condensation and apoptotic body formation with elevated DPA levels suggesting DNA damage in HepG2 cells. DNA damage assessed by the comet assay confirmed an increased comet tail formation. The presence of oxidative stress was investigated by quantifying reactive species (malondialdehyde and nitrates concentration) and Western blotting to confirm the expression of antioxidant proteins. The DPA increased lipid peroxidation (RNS), a marker of oxidative stress, consequently causing cell death. The accompanying upregulation of stress‐associated proteins superoxide dismutase (SOD2), nuclear factor (erythroid‐derived 2)‐like 2 (Nrf2), and Hsp70 verifies oxidative stress.
    Type of Medium: Online Resource
    ISSN: 0885-4513 , 1470-8744
    URL: Issue
    URL: Article
    DOI: 10.1002/bab.v68.2
    DOI: 10.1002/bab.1918
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 1496341-3
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Toxicogenicity and mechanistic pathways of aflatoxin B1 induced renal injury
    Wiley ; 2021
    In:  Environmental Toxicology Vol. 36, No. 9 ( 2021-09), p. 1857-1872
    Details
    In: Environmental Toxicology, Wiley, Vol. 36, No. 9 ( 2021-09), p. 1857-1872
    Abstract: The study investigated the toxicogenic effects, molecular mechanisms and proteomic assessment of aflatoxin B 1 (AFB 1 ) on human renal cells. Hek293 cells were exposed to AFB 1 (0–100 μM) for 24 h. The effect on cell viability was assessed using the methylthiazol tetrazolium (MTT) assay, which also produced the half maximal inhibitory concentration (IC 50 ) used in subsequent assays. Free radical production was evaluated by quantifying malondialdehyde (MDA) and nitrate concentration, while DNA fragmentation was determined using the single cell gel electrophoresis (SCGE) assay and DNA gel electrophoresis. Damage to cell membranes was ascertained using the lactate dehydrogenase (LDH) assay. The concentration of ATP, reduced glutathione (GSH), necrosis, annexin V and caspase activity was measured by luminometry. Western blotting and quantitative PCR was used to assess the expression of proteins and genes associated with apoptosis and oxidative stress. The MTT assay revealed a reduction in cell viability of Hek293 cells as the AFB 1 concentration was increased, with a half maximum inhibitory concentration (IC 50 ) of 32.60 μM. The decreased viability corresponded to decreased ATP concentration. The upregulation of Hsp70 indicated that oxidative stress was induced in the AFB 1 ‐treated cells. While this implies an increased production of free radicals, the accompanying upregulation of the antioxidant system indicates the activation of defense mechanisms to prevent cellular damage. Thus, membrane damage associated with increased radical formation was prevented as indicated by the reduced LDH release and necrosis. In addition, cytotoxic effects were evident as AFB 1 activated the intrinsic pathway of apoptosis with corresponding increased DNA fragmentation, p53 and Bax upregulation and increased caspase activity, but externalization of phosphatidylserine (PS), a major hallmark of apoptosis, did not occur in AFB 1 treated renal cells. The results suggest that AFB 1 induced oxidative stress leading to cell death by the intrinsic pathway of apoptosis in renal cells.
    Type of Medium: Online Resource
    ISSN: 1520-4081 , 1522-7278
    URL: Issue
    URL: Article
    DOI: 10.1002/tox.v36.9
    DOI: 10.1002/tox.23306
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2027534-1
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  • 4
    Online Resource
    Online Resource
    Risk factors for amyotrophic lateral sclerosis: A regional United States case‐control study
    Wiley ; 2021
    In:  Muscle & Nerve Vol. 63, No. 1 ( 2021-01), p. 52-59
    Details
    In: Muscle & Nerve, Wiley, Vol. 63, No. 1 ( 2021-01), p. 52-59
    Abstract: Most amyotrophic lateral sclerosis (ALS) cases are considered sporadic, without a known genetic basis, and environmental exposures are thought to play a causal role. To learn more about sporadic ALS etiology, we recruited n = 188 ALS patients from northern New England and Ohio and matched controls 2:1 from the general population of the same regions. Questionnaires evaluated the association between a variety of lifestyle, behavioral (ie, hobbies and activities), and occupational factors and the risk of ALS, including the duration of time between exposure and ALS onset, and exposure frequency. Head trauma was associated with increased ALS risk (adjusted odds ratio [OR] 1.60 95% confidence interval [CI] 1.04‐2.45), with significantly greater effects for injuries occurring 10 or more years prior to symptom onset ( P = .037). ALS risk was increased for those reporting severe electrical burns (adjusted OR 2.86, 95% CI 1.37‐6.03), with odds ratios highest for burns after age 30 (OR 3.14), and for burns 10 or more years prior to symptom onset (OR 3.09). Hobbies involving lead were the most strongly associated with ALS risk (adjusted OR 2.92, 95% CI 1.45‐5.91). Exposures to lead 20 or more years prior to diagnosis had larger effect sizes compared to those occurring more recently. Holding a job in mechanics, painting, or construction was associated with ALS. The identification of these specific environmental factors associated with ALS highlight the need for future prospective and laboratory studies to assess causality, biological mechanisms, and find prevention or treatment opportunities.
    Type of Medium: Online Resource
    ISSN: 0148-639X , 1097-4598
    URL: Issue
    URL: Article
    DOI: 10.1002/mus.v63.1
    DOI: 10.1002/mus.27085
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 1476641-3
    SSG: 12
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