Cellular divisions

Colmano, G. 1973. Molybdenum toxicity abnormal cellular division of teratogenic appearance in Euglena gracilis. Bull. Environ. Contam. Toxicol. 9 361-364. 

Nickel chloride has been reported to induce DNA strand breaks in CHO cells [435] in a concentration, which did not significantly injure normal cellular division, and DNA-protein cross-links, which were concentration- and time-dependent and preferentially occurred in cells in the late S phase of the cell cycle [436], The nickel cross-linked proteins included nonhistone chromatin proteins, nonhistone DNA-binding proteins and a 30 kDa protein that comigrated electrophoretically with histone HI. Moreover, blocking of cell growth in S phase [249] and induction of DNA repair synthesis in CHO cells [437] and reduction in the fidelity of DNA synthesis [438, 439], have been reported. 

Another factor that requires to be taken into account is the intrinsic variability of organisms within what is in effect a mixed culture. There are different species of organism present and even the same species will have cells at different stages of cellular division. Some cells in a mixed system will be very susceptible to the applied stress and others will be more resistant. Obviously it is the resistant cells that will require sufficient stress to kill them, no matter how that term is applied. Filtration to remove as many microorganisms as possible before any sterilizing stress is applied is clearly a sound practice. 

Unfortunately, cancerous cells are not the only cells in the body that divide. Normal cells divide periodically, and some types of cells, such as those in the gastrointestinal tract and in hair follicles, are always in a state of cellular division. As a consequence, cancer chemotherapeutics are noted for their toxicity, with patients undergoing treatments often experiencing gastrointestinal problems and hair loss. 

Cruz-Ortega, R., Anaya, A.L., and Ramos, L. Effects of allelopathic compounds of maize pollen on respiration and cellular division of watermelon. J Chem Ecol 1988 14 71-86. 

T Tamura, H Suzuki, Y Nishimura, J Mizoguchi, Y Hirota. On the process of cellular division in Escherichia coli isolation and characterization of penicillin-binding proteins la, lb, and 3. Proc Natl Acad Sci (USA) 77 4499-4503, 1980. 

M Ricard, Y Hirota. Process of cellular division in Escherichia coli physiological study on thermosensitive mutants defective in cell division. J Bacteriol 116 314— 322, 1973. 

To solve Equation 93 it is necessary to know the characteristic functions of the cellular physiology, that is, the growth rate r(m, S), the cellular division rate T(m, S), and the cell mass partition function p(m, m, S). Since these functions are substrate concentration- dependent, the substrate consumption rate must also be defined. These substrate concentration variations are calculated using the yield coefficient Yx/s, that establishes a relationship between the growth rates and the substrate consumption rate. The consumption rate is indicated by Equation 94. 

Chronic low-level exposure to As may stimulate growth of cells that produce keratin, leading to increased cellular division (and accompanying DNA replication) that creates allows greater opportunities for genetic damage. 

The action on cell components results in inhibition of cellular division (mitosis) with decreased tissue respiration that leads to cell death. It produces eye, airway, and skin and mucous membrane injury that can be fatal. Systemic effects with extensive exposures include bone marrow inhibition with a drop in the white blood cell count and gastrointestinal tract damage. 

Antimetabolites compete with normal endogenous substrates and cause inhibition of the processes that require those substrates. Examples include purine and pyrimidine antagonists, which prevent nucleic acid replication and cellular division in cancer chemotherapy. Another example is methotrexate, which can inhibit folic acid metabolism. 

Excessive inflammatory responses may result from inappropriate cellular signaling. On the other hand, inflammation is normally a protective response, and its lack can lead to increased susceptibility to infections. Dysregulation of cellular division can lead to neoplasia or aplasia. Neoplastic changes reflect a dysregulation of cell growth, whether from failure of apoptosis or other mechanisms. 

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