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Ayyalasomayajula Neelima, Ajumeera Rajanna, Reddy G. Bhanuprakash, C.S. Chetty and Challa Suresh

Abstract

Lead (Pb) is a toxic pollutant known to cause several abnormalities related to the brain, including cognitive dysfunction, and it is ubiquitous in nature. β-amyloid peptides (AP) are crucially involved in Alzheimer’s disease (AD). It has been reported that there is a connection between lead and amyloid peptides in exerting similar kinds of altered functions in the brain and long-term exposure to lead leads ultimately to increased beta amyloid formation in the brain, lethal to human brain cells. There is still a lack of information on the mechanism by which Pb affects AP formation, exerting combined toxicity in AD patients. To fill the gap, we have systematically analyzed the toxicity individually and in combination of Pb and AP in human brain cells. We found that the combination of Pb and AP exerted a higher toxicity than individual exposures in human neuroblastoma cells. The lower inhibitory concentration values were determined by both time and concentration dependent manner on using MTT assay. The data resulted in the development of enhanced toxicity on exposure to Pb with both the combinations of AP(1-40) or (25-35) and with all combinations in human brain cells compared to individual exposures to Pb (1-40) or AP(25-35). The severe apoptotic effect and alteration in cell cycle by arresting at the S-phase evidenced the increased toxicity of combinational exposure to Pb and AP on human neuroblastoma cells. Furthermore, the quantitative determination of LDH and caspase-3 activity indicated the induction of severe toxicity. We conclude that both are synergistically associated with effects such as arresting the cell cycle and triggering apoptosis during the progression of Alzheimer’s disease.

Open access

Ashim Kumar Basak, Tridip Chatterjee, Swapan Kumar Ghosh and Amit Chakravarty

Abstract

The effects of four food additives, namely sodium nitrite (NaNO2), sodium nitrate (NaNO3), potassium nitrite (KNO2), and potassium nitrate (KNO3), on animal development were evaluated by using Drosophila melanogster, a model organism. Adult male and female flies were allowed to breed in culture medium, each containing one of 4 concentrations, i.e.10, 20, 30 or 40 mM of the above mentioned salts. The concentration of 40 mM, NaNO2 and KNO2 completely arrested the development of the flies. Of the different concentrations of the four salts tested, exposure of flies to 30 mM NaNO2 exhibited only significant delays in the initial appearances of third instar larvae, pupae and young adults, along with huge reduction in the number of pupae and young adults compared to controls. Rearrangements like inversions, deletion looping, regional shrinking, as well as highly enlarged puffing, etc. were also observed in the polytene chromosomes of the third instar larvae exposed to 30 mM NaNO2. Developmental outcomes of the flies exposed to varying concentrations of NaNO3 and KNO3 did not differ significantly from the controls. Owing to the extensive genetic homology between Drosophila and human and the successful uses of this fly as models in developmental and toxicological studies, we speculate that the experimental results exhibited by this organism in our study strongly advocate for abstaining from the dietary use of NaNO2 and KNO2 during human pregnancies to avoid possible negative developmental outcomes.

Open access

Eduard Ujházy, Mojmír Mach, Jana Navarová, Ingrid Brucknerová and Michal Dubovický

ABSTRACT

Teratology is the science that studies the causes, mechanisms, and patterns of abnormal development. The authors present an updated overview of the most important milestones and stages of the development of modern teratology. Development of knowledge and society led to the recognition that causes of congenital developmental disorders (CDDs) might be caused by various mechanical effects, foetal diseases, and retarded or arrested development of the embryo and foetus. Based on the analysis of the historical development of hypotheses and theories representing a decisive contribution to this field, we present a survey of the six Wilson´s fundamental principles of teratology. The aim of observing these principles is to get insight into developmental relations and to understand mechanisms of action on the level of cell populations (elementary morphogenetic processes), tissues and organs. It is important to realise that any negative intervention into the normal course of these processes, either on genetic or non-genetic basis, inevitably leads to a sequence of subsequent changes resulting in CDDs. Moreover, the classical toxicologic monotonic doseresponse paradigm recently has been challenged by the so-called “low dose-hypothesis”, particularly in the case of endocrine active substances. These include some pesticides, dioxins, polychlorobiphenyls (PCBs), and bisphenol A. Despite modern approaches of molecular biology and genetics, along with top diagnostic techniques, we are still not able to identify the actual cause in more than 65 to 70% of all congenital defects classified as having an unknown etiology. Today CDDs include any birth defect, either morphological, biochemical, or behavioural.

Open access

Martina Melušová, Soňa Jantová and Eva Horváthová

LS, Chan KW, Tahir PM, Ismail M. (2013). Kenaf seed oil from supercritical carbon dioxide fl uid extraction induced G1 phase cell cycle arrest and apoptosis in leukemia cells. Afr J Biotech 10: 5389-5397. Higuchi Y. (2003). Chromosomal DNA fragmentation in apoptosis and necrosis induced by oxidative stress. Bioch Pharm 66: 1527-1535. Horvathova E, Navarova J, Galova E, Sevcovicova A, Chodakova L, Snahnicanova Z, Melusova M, Kozics K, Slamenova D. (2014). An Assessment of Antioxidative, Chelating and DNA-protective Eff ects of

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Marie Stiborová, Jitka Poljaková, Eva Martínková, Lucie Bořek-Dohalská, Tomáš Eckschlager, Rene Kizek and Eva Frei

. Characterization of enzyme-drug interactions by fluorescence spectroscopy. J Biol Chem   270 : 4998-5004. Kuo PL, Hsu YL, Chang CH and Lin CC. (2005a). The mechanism of ellipticineinduced apoptosis and cell cycle arrest in human breast MCF-7 cancer cells. Cancer Lett   223 : 293-301. Kuo PL, Hsu YL, Kuo YC, Chang CH and Lin CC. (2005b). The antiproliferative inhibition of ellipticine in human breast mda-mb-231 cancer cells is through cell cycle arrest and apoptosis induction. Anti-Cancer Drugs   16 : 789

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Tomáš Perečko, Katarína Drábiková, Radomír Nosáľ, Juraj Harmatha and Viera Jančinová

). Oxidantmediated phosphatidylserine exposure and macrophage uptake of activated neutrophils: possible impairment in chronic granulomatous disease. J Leukoc Biol 71 : 775-781. Horvath Z, Marihart-Fazekas S, Saiko P, Grusch M, Ozsuy M, Harik M, Handler N, Erker T, Jaeger W, Fritzer-Szekeres M, Djavan B and Szekeres T. (2007). Novel resveratrol derivatives induce apoptosis and cause cell cycle arrest in prostate cancer cell lines. Anticancer Res 27 : 3459-3464. Jančinova V, Drabikova K, Nosaľ R, Račkova L, Majekova M, Holomańova D. (2006). The

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Petr N. Menshanov and Andrey E. Akulov

. (2003). Hypothermia-induced respiratory arrest and recovery in neonatal rats. Respir Physiol Neurobiol 137 : 29–40. Tkác I, Rao R, Georgieff MK, Gruetter R. (2003). Developmental and regional changes in the neurochemical profile of the rat brain determined by in vivo 1H NMR spectroscopy. Magn Reson Med 50 : 24–32. Tomiyasu M, Aida N, Endo M, Shibasaki J, Nozawa K, Shimizu E, Tsuji H, Obata T. (2013). Neonatal brain metabolite concentrations: an in vivo magnetic resonance spectroscopy study with a clinical MR system at 3 Tesla. PLoS One 8 : e82746

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Soňa Jantová, Dominika Topoľská, Michaela Janošková, Miroslav Pánik and Viktor Milata

kinase CK2. J Med Chem 49: 6443-6450. Hadjeri M, Peiller E, Beney C, Deka N, Lawson M, Dumontet C, Boumendjel A, (2004). Antimitotic activity of 5-hydroxy-7-methoxy-2-phenyl-4-quinolones. J Med Chem 47: 4964-4970. Huang L, Hsieh M, Teng C, Lee K, Kuo S. (1998). Synthesis and antiplatelet activity of phenyl quinolones. Bioorg Med Chem 6: 1657-1662. Chang Y, Yang J, Kuo S, Chung J. (2009). Induction of mitotic arrest and apoptosis by a novel synthetic quinolone analogue, CWC-8, via intrinsic and extrinsic apoptotic pathways

Open access

Gianpaolo Guzzi, Paolo D. Pigatto, Francesco Spadari and Caterina A.M. La Porta

, Lee TJ, Bae JH, Jang BC, Song DK, Cho JW, et al. Thimerosal induces apoptosis and G2/M phase arrest in human leukemia cells. Mol Carcinog 45 : 657-666. Bahia Mde O, De Amorim MI, Burbano RR, Vincent S, Dubeau H. (1999) Geno-toxic ef ects of mercury on in vitro cultures of human cells. An Acad Bras Cienc 71 : 437-443. Ogura H, Takeuchi T, Morimoto K. (1996) A comparison of the 8-hydroxyde-oxyguanosine, chromosome aberrations and micronucleus techniques for the assessment of the genotoxicity of mercury compounds in human blood

Open access

Rado Nosáľ, Katarína Drábiková, Viera Jančinová, Tatiana Mačičková, Jana Pečivová, Tomáš Perečko and Juraj Harmatha

, CňHo CT. (2007). Pterostilbene induces apoptosis and cell cycle arrest in human gastric carcinoma cells. J Agricult Food Chem 55 : 7777–85. Pan MH, Chiou YS, Chen WJ, Wang JM, Badmaev V, Ho CT. (2009). Pterostilbene inhibited tumor invasion via suppressing multiple signal transduction pathways in human hepatocellular carcinoma cells. Carcinogenesis 30 : 1234–42. Pečivová J, Mačičková T, Lojek A, Gallová L, Číž M, Nosáľ R, Holomáňová D. (2007). In vitro effect of carvedilol on professional phagocytes. Pharmacol 79 : 86–92. Perečko T