TOXIC SUBSTANCES A neurotoxin is any form of exogenous chemical whose introduction in the body will result inan adverse effect on the functioning of the nervous system cells in both developing and mature states. Neurotoxins specifically target components of the neurological part of the body, resulting in their destruction. Arsenic is one such compound. It exists in both organic and inorganic form in air, soil and water with the organic form found in fish and shellfish regarded as less toxic (CDC, 2011). However, it is mostly found in areas subject to mining, smelting and agricultural run-off. Ingestion of arsenic in the development stage of the nervous system results in the neurites’ growth being inhibited (CDC, 2011). This is due to the formation of arsenite, which is an arsenic metabolite that forms within 24 hours of ingestion. The arsenite toxic mechanism is to create an increased level of calcium ion levels between neurons that causes the transmembrane potential of the mitochondria to reduce which brings about death of the cell as an eventuality due to caspases (CDC, 2011).
Many drugs may result in the manifestation of cardiovascular effects in the form of changes in blood pressure and heart rate (Kacew &amp. Lee, B. 2013). However, the ingestion of some of these substances in significant amounts may result in them having toxic characteristics of the cardiovascular system. Digoxin is one such compound. This is a form of cardiac glycoside that is purified after the extraction from the foxglove plant. The compound is used in the treatment of heart diseases in regulating amounts. However, acute over dosage results in the development of marked bradycardia with the prolongation of the QRS and PR (Thanacoody &amp. Waring, 2008). The toxicity of the compound is similar to arsenic as it affects concentrations of calcium in cells. The compound introduction to the cardiovascular system in vast quantities results conducting and myocardial tissues’ inhibition of ATPase pump of Na+/K+ (Thanacoody &amp. Waring, 2008). This property leads to a reduction in the intracellular efflux of calcium through the exchange mechanisms of Na+/Ca2+. The effect is an increase in the calcium intracellular concentrations. That manifests in the form of marked bradycardia (Thanacoody &amp. Waring, 2008). It is also associated with sinus arrests and haemodynamic instability due to varying atrioventricular block degrees.
Cadmium is also a toxic substance to the body. However, its toxicity has to do with the endocrine system. The endocrine system is the system of glands and organs that secrete hormones that regulate the body’s homeostasis. Cadmium is a heavy metal that is sourced from aerosols, mines water wastes and phosphate based fertilizers (Georgescu et al., 2011). Like arsenic, the compound is found in air, water and soil with documentations showing the compound concentrations peak 0.003mg Cd/m3 in industrial areas. We are normally in environments that contain cadmium in low levels. However, the metal’s toxic properties are not exhibited when it is found in the body in small amounts. The accumulation of the metal in the body over a period of around 20 years results in it being metabolized (Georgescu et al., 2011).
This causes the metal to settle in various organs in the body like the kidney, liver hair and blood. Although the metal is found in higher concentrations among males, when it settles in the hormone secreting organs, it inhibits the working of the organs resulting in the low levels of the homeostasis regulating hormones (Georgescu et al., 2011). The effect is that the body is not able to carry out activities necessary to remove wastes and toxins from the body, leading to death of cells, organ failure and eventually death. The metal also results in the development of cancer cells in organs where it has accumulated (Georgescu et al., 2011).
CDC,. (2011). Arsenic Health Effects. Retrieved from
Georgescu, B., et al. (2011). Heavy metals acting as endocrine disrupters. Scientific Papers Animal Science And Biotechnologies, 44(2), 89–93.
Kacew, S., &amp. Lee, B. M. (2013). Lus basic toxicology: Fundamentals, target organs, and risk assessment (6th ed.). New York, NY: Informa Healthcare.
Thanacoody, H., &amp. Waring, W. (2008). Toxins that affect the cardiovascular system. Clinical Medicine, 8(1), 92–95.

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