Response to hypoxic stress

The exposure to low levels of oxygen (hypoxic conditions) can result in decreased cell survival in many animals. C. elegans has an preferred range of oxygen concentration and reacts on a cellular level to drops in environmental oxygen concentrations through a hypoxia response pathway. Since the induction of hypoxic conditions has been correlated with a mechanism of attack used by pathogenic bacteria, this response pathway also helps C. elegans defend itself against microbial attack.

Hormesis

The process whereby a low exposure to a toxin or stressor produces a generally positive response in the animal that is the opposite effect produced in response to a higher exposure. This can be observed in cases where C. elegans is exposed to short doses of temperature stress during development. Under such limited exposures, animals exhibit a longer life span than animals reared at room temperature. However, extended exposure to thermal stress results in severely shortened lifespans.

Neurotransmission

Neurons communicate across synaptic junctions with target cells, such as neurons, muscles, or specialized secretory cells through chemical messengers that are released from the neuron and bind to and activate receptors on the target cell. Pre-synaptic release of neurotransmitters can be evoked, such as through mechanical or chemical stimulation, as well as can occur spontaneously at a low rate. Depending on the neurotransmitter released and or the receptors of the post-synaptic cell, the activation of receptors can trigger excitatory or inhibitory actions in the target cell. These neuronal communications can also result in short term post-synapatic cellular changes to the membrane potential or can cause the activation of signaling cascades, resulting in longer term changes in the cell.

Response to metal

Some chemical metals are micronutrients at low concentrations and are essential for key biological processes. At higher concentrations, these essential metals, e.g., calcium (Ca), copper (Cu), zinc (Zn), manganese (Mn), etc., can have toxic effects. Likewise, nonessential metals, even in low doses can also be toxic. Toxicity can be attributed to the metal element binding to structural proteins, enzymes, and nucleic acids, inhibiting or altering the function of the bound object. Both essential and nonessential metals are found naturally in the environment as well as in concentrated sources stemming from human activity through mining and industrial wastes; vehicle emissions; lead-acid batteries; fertilizers, paints and treated woods. Metals, in particular heavy metals such as cadmium (Cd), arsenic (As), antimony (Sb), lead (Pb), mercury (Hg), and chromium (Cr), have been shown to be able to impede or alter basic cellular functions causing severe neurological damage. C. elegans, the most abundant soil invertebrate, provides a model organism for the study of metal toxicity. As a free-living soil nematode, C. elegans is exposed to many toxins naturally present in the soil. Heavy metals such as Cd result in larval lethality and arrested development. Among its repertoire of defenses, C. elegans has a highly tuned nervous system that allow the animals to recognize and avoid toxins, for example the ADL, ASE and ASH neurons direct behaviors in response to Cu or Cd. In cases of exposure to toxic concentrations of metals, a generalized cellular stress response is activated that includes an increase in expression of a number of genes, including heat shock stress proteins such as daf-21/Hsp90, that direct cellular repair and defense. Studies of metal toxicity in C. elegans has also revealed a strong correlation between toxicity and temperature-dependent metabolic activity.