The Effect Of Cisplatin On Cell Division Of Escherichia Coli Bacteria

that the old cells don’t die but new and abnormal ones start growing. These cells grow together

This allows it to interact with other atoms in many ways. This is very significant when Platinum is used in anticancer drugs for chemotherapy. Cisplatin is a Platinum based drug and is one of the oldest and most successful anticancer drug in the history of chemo prescriptions. The molecule structure of DNA is very important for the interaction of Cisplatin. It is a double-helix and is held together by building blocks, scientifically known as nucleotides. Through the bases of DNA, Platinum is then able to its job. The drug reacts in a displacement reaction. The chlorine atoms that are in our bodies are displaced by the aqua ligand, a coordination compound of metal ions and water, which is the displaced by the nitrogen in the DNA. The cisplastin then is left to interact with the DNA and creates two cross-link stands. Repairing mechanisms in the body then separate the cisplastin from the DNA which then causes the damage of the unhealthy cells. (Carmen Drahl 2017) this is shown in fig

The body is made up of hundreds of millions of living cells. Normal body cells grow, divide, and die in an orderly fashion. During the early years of a person’s life, normal cells divide faster to allow the person to grow. After the person becomes an adult, most cells divide only to replace worn-out or dying cells or to repair injuries. Cancer begins when cells in a part of the body start to grow out of control. There are many kinds of cancer, but they all start because of out-of-control growth of abnormal cell (American Cancer Society, 2010).

DNA can get damaged. If and when this does happen to a normal cell a new cell will repair the damage. If the cell does not repair the damaged DNA cell the damaged cell will automatically die and the new cell will replace its spot. Sometimes the DNA damage is not repaired and the cell will still live becoming an abnormal cell. Abnormal cells can keep multiplying even though the body doesn’t need more cells. Those cells still have damaged DNA therefore the uncontrollable cell growth will keep on repeating. Think of cancer starting as a party. The cells don't want to stop to turn down the music or stop joining the

Cytotoxic chemotherapy was first discovered during World War II by Gilman and Philips when they perceived the effect that nitrogen gas (used during WWI) had on the number of human cells proliferating and recognised this as a potential treatment for cancer. From this discovery, biotherapy was born helping to increase our knowledge in how to achieve cell death and tumour control through use of cytokines and monoclonal antibodies (Young et al, 2006). Cancer is often described as unregulated cell growth through a multistep process (Brighton et al, 2005). Brighton (2005) describes the ‘Hallmarks’ of the cancer cell as needing to acquire these six steps in order to develop: ‘self-sufficiency in growth signals, insensitivity to antigrowth signal, avoiding apoptosis, limitless replicative potential, angiogenesis and tumour invasion/ metastasis’. These six Hallmarks of Cancer describe the pathogenesis that a cell undertakes until it develops into a tumour which can then potentially become malignant (Hanahan et al, 2011). While normal cells can control their own proliferation that allows a homeostasis amongst cells, that new cells are born once the old cells have died ensuring that there are enough cells available to fulfil the task at hand. Cancer cells are more neurotic, they interrupt the normal signalling pathway within the healthy cells, and then they begin to grow uncontrollably invading the

An irritant, such as cigarette smoke, effects the cells of the epithelium lining. Initially the body can repair the cell, but with repeated exposure the cells of the lungs become damaged and grow uncontrollably. P53 is a gene for various downstream targets that are involved in cell progression, DNA repair and regulation of cells that undergo apoptosis. Mutations to P53 hinder its normal tumor suppressing capabilities. Therefore, DNA damage remains unchecked, faulty cells proceed through the cell cycle and apoptosis is invaded. All these factors create a genetic condition where the cell is more susceptible to further mutation. If the cancer grows large enough, it can affect the organ by closing off the aveoli, leading to shortness of

Since its discovery four decades ago, cisplatin has been widely used for chemotherapy showing a potent activity against a broad spectrum of tumors and demonstrating one of the highest cure rates (Kart et al., 2010; Yousef et al., 2009; Wang and Lippard, 2005). Cisplatin cytotoxic effects result mainly from its interaction with DNA via the formation of covalent adducts between certain DNA bases and the platinum (Yang et al., 2006). Unfortunately, cisplatin treatment is plagued by many problems including resistance, both intrinsic and acquired, and strong side effects such as nephrotoxicity, cardiotoxicity, ototoxicity, neurotoxicity, and emetogenesis (Kartalou and Essigmann, 2001; [2]).

So what exactly is causing the cells to not properly divide and die? Well the cells center, the nucleus, is responsible for commanding the cells functions, but it doesn’t always send the right orders. So the question know becomes, why doesn’t the nucleus send the right commands?

Breast cancer is a disease that starts when an abnormal, uncontrolled cell growth occurs in the tissues of the breast. In a healthy body, cells grow, divide, and die in an orderly way, but once a damage or a mutation happens in the genetic material of the cell (which is found in the DNA) it results in cells that do not die. They continue to grow and divide uncontrollably and form abnormal cells that the body does not need. They can also metastasize, which means they invade other tissues through the bloodstream or lymph vessels. In contrast, in normal cells, when DNA is damaged the cell either repairs the damage or dies (Sudhakar 2009).

- However, when cancer develops, the cells become irregular, the old cells that should die but

Oxaliplatin inhibits DNA synthesis, primarily by conforming DNA adducts. Oxaliplatin, a platinum compound, has a broad spectrum of anti-tumor activity and has demonstrated a lack of cross-resistance with other platinum compounds. Oxaliplatin induces primary and secondary DNA lesions that lead to cell apoptosis.

The cells of a multicellular organism are members of a highly-organized community. The number of cells in this community is regulated, not by controlling the rate of cell division, but also by controlling the rate of cell death. If cells are no longer needed, they commit suicide by activating an intracellular death program. This process is therefore called programmed cell death, although it is more commonly called apoptosis. Cell death plays a role in development and the process is called, morphogenesis, the biological process that causes an organism to develop its shape. It also plays a role in the maintenance

The regulation of cell growth and differentiation is critical to the survival of multicellular organisms. Typically cells growth is tightly regulated. Precursor cells will proliferate and differentiate into mature cell types. Upon differentiation to the terminal, mature cell type, cells would then enter into stasis, or quiescence. In quiescence cells stop dividing and perform their cellular function. Quiescent cells no longer grow or proliferate. If cells become damaged, are no longer useful, or for some other reason need to be eliminated cells will undergo a regulated cell death process called apoptosis. Neoplasia is the process of Inheritable changes in cell growth that have lost normal control processes. , at the cellular level, autonomous

In 1965 Barnett Rosenberg made the accidental discovery of the biological use cisplatin whilst conducting an experiment on the effects of electrical current on the bacterial E.coli (Escherichia coli). When the electrical current was turned on, it was observed that the cell division was inhibited causing a decline in the density of the bacterium. However, when the electrical field was turned off, the bacterium returned to its normal density. It was later found that the inhibition of cell division was not due to the electrical current but rather the production of cis- diamminedichloroplatinum (IV) from the platinum electrodes. The trans isomer of the compound was found to be inactive at low concentrations. Other group 10 metal complexes were tested and similar results, however the most effective remained to be the platinum complex. The discovery of this lead to the interest of testing these complexes for their anticancer behaviour. So the platinum (II), cis-[PtCl2(NH3)2], complex and the platinum (IV), cis-[PtCl4(NH3)2] were tested against the Sacroma 180 tumours of Swiss white mice. The complexes showed effective anticancer activity. The large solid tumours were shrunk and the mice lived and they were healthy. The study was so successful the mice even lived another 6 months without any signs of the cancer. This study was the basis in which cisplatin entered clinical trials and have now become one of the most successful anticancer drugs in medicine.

Cell death is when a biological cell stops carrying out is function. Cell death can be due to the natural process of replacing old cells with new ones, or may result from factors such as disease, localized injury, or even death of the whole organism.