Hormesis examples

For example, mitochondrial reductive capacity is decreased with decreased cell numbers but is increased with cells that are activated, such as lymphocytic immune activation, or if cells adapt to the stress associated with toxicity, such as during mitochondrial biogenesis. Thus, mitochondrial reductive capacity might be either increased or decreased with toxicity. Similar contradictory interpretations might occur with other cellular activities, for which there is a compensatory adaptive increase before their failure. This biphasic change is referred to as hormesis and occurs not only with reductive mitochondrial activity but also with mitochondrial number, cell number, mitochondrial membrane potential, antioxidant system activity and numerous other activities. 

Dichotomous responses. Some endpoints (e.g., behavioral parameters) can lead to nonmonotonous concentration-response curves, which are more difficult to model than the monotonous concentration-response curves that are observed, for example, in survival studies. Also in case of hormesis, nonmonotonous concentration-response curves are found. Nonmonotonous curves pose inherent problems for the application of both mixture toxicity concepts (Backhaus et al. 2004 Belz et al. 2008). 

Figure 3 Stylized dose-response curves reflecting the relative distribution of stimulatory dose ranges. Note the maximum stimulatory response is usually 130%—160% of the control value regardless of the width of the stimulatory dose range the inverted U-shaped curve was used for illustrative purposes only, whereas examples in the hormesis database include both inverted U- and U-(J-) shaped curves depending upon the endpoint measured. Modified from Calabrese (30).

Toxic action is concentration dependent. For example, phenol can be metabolized at low concentrations but becomes toxic at higher concentrations. These types of actions often lead to the occurrence of a hormesis effect, i.e. the stimulating effect of small doses of a toxicant that is known to be inhibitory at larger concentrations. Toxicant action also depends on the presence of other chemicals in solution (Dutka and Kwan, 1982). 

The hormesis databases developed by Calabrese and his colleagnes are snp-portive of the EPA mode of action and weight of evidence. For example, they are consistent (in fact, essential) to meet the EPA s requirement of a weight-of-evidence narrative that should describe and be intelligible to risk managers and nonexpert readers (EPA 2005) regarding ... 

Since thousands of examples of hormesis-like biphasic dose-responses exist in highly diverse biological systems, it is likely that there is no single proximate mechanistic... 

Although most endpoints are amenable to a hormesis evaluation, some commonly assessed endpoints are inherently problematic. For example, serum enzyme activities such as those routinely taken to assess liver toxicity, such as ALT and AST, would not be a means to study hormesis because any changes from normal, whether high or low, may be indicative of some underlying pathology. In order to assess whether liver changes would be reflective of a hormetic response it may be necessary to utilize an animal model with a high predisposition to liver disease or to create experimental conditions that would promote the early onset of liver disease. 

Hormesis is a dose-response phenomenon characterized by low-dose stimulation and high-dose inhibition. The determination of whether the hormetic stimulation is beneficial or not should be decoupled from a decision as to whether the response is hormetic or not. Hormetic effects themselves can be beneficial, neutral, or harmful depending on the specific circumstances. For example, a low-level exposure to an antibiotic may stimulate the growth of harmful bacteria that could be harmful to human patients yet theoretically... 

Is the J-shaped dose response that is widely reported for alcohol consumption and various types of cardiovascular disease an example of hormesis Why or why not Explain. 

The second hypothesis states that there is a threshold below which no harm accrues, and, further, that lower doses may even be beneficial. When a toxin at high levels is beneficial at low levels, it is called hormesis. Substances exhibiting hormesis are, for example, vitamin D, selenium, aspirin, table salt, water, and, for plants, fertilizer. There may even be a hormesis effect for low-level radiation because this might provide the stimulus for the heighteued activity of DNA repair mechanisms (Karam, 2003). 

The above examples are just a few of the many studies that have shown that radiation health effects demonstrate a hormetic effect, a characteristic of most pharmaceuticals and even to many foods. Hormesis is the concept that large doses of a substance may be detrimental to health, but small doses are beneficial. The evidence for this knowledge was effectively presented in a text published in 1980, titled Radiation Hormesis, by Dr. T.D. Luckey, and in 1991 followed by the second edition [7]. This text included over 1000 references of data on radiation hormesis. 

Except for the example of falcarinol, no systematic attempts have been made to determine the net impact of these compounds on health. Until now, almost all experiments have been one-sided designs where either toxic or beneficial effects could be assessed but not both. Another problem has been that the dose-response dependencies have often been assumed to be linear, so the range of concentrations used in the studies did not cover levels corresponding to the actual normal intake from food, since the possibility of hormesis has only recently received significant attention. A third issue, which is generally... 

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