Answer:
A) Decreases cellular energy production
B) DCCD also affects K+ transport
Explanation:
A) Consequences are of DCCD on cellular energy production: <em>Decreases cellular energy production</em>
ATP-synthase pump is composed of two subunits: F1 catalytic subunit that synthesizes ATP, and F0 proton pumping subunits, that transport H+ through the membrane. F1 subunit might act independently of F0 to produce ATP, but this molecule can not be released without H+ gradient, which generates a movement necessary for ATP release from the catalytic center.
When any of the parts composing F0 react with DCCD, the subunit can not transport H+ through the membrane. DCCD inhibits the enzyme activity by blocking the protons´ flow.
As DCCD blocks the protons´ flow, and the protons´ flow is necessary to release the ATP molecule from the F1 subunit, no other ADP + Pi can enter to F1 subunit, and the production of ATP stops.
B) Other cellular effects of DCCD
There seem to be other effects of DCCD on cell activity, some of which are still under study. To name a few:
- Diimide from DCCD seems to stimulate cytochrome b reduction and inhibits its reoxidation by ferricyanide.
- When exposing the cell to high concentrations of DCCD for a long time, might occur an alteration in the electron transporting chain
- Inhibition of ubiquinol-cytochrome c reductase activity when exposing the cell to high concentrations of DCCD.
- Inhibition of K+ transport, associated with the inhibition of H+ transport.
Concerning the effect of DCCD on the K+ transport, DCCD stops the extrusion of H+ and the consequent intrusion of K+.
DCCD strongly inhibits the simultaneous flow of H+ and K+. First, it inhibits H+ flow, acidification of the environment stops, but at this point, K+ keeps moving through the membrane. Once the H+ flow has ceased, the K+ flow slowly decreases until it finally stops moving. There is a lag time in the DCCD effect on K+ flow to the instantaneous effect on H+ flow.
<span>Rhabdomyolysis constitutes a common cause of acute renal failure and presents paramount interest. A large variety of causes with different pathogenetic mechanisms can involve skeletal muscles resulting in rhabdomyolysis with or without acute renal failure. Crush syndrome, one of the most common causes of rhabdomyolysis presents increased clinical interest, particularly in areas often involved by earthquakes, such as Greece and Turkey. Drug abusers are another sensitive group of young patients prone to rhabdomyolysis, which attracts the clinical interest of a variety of medical specialties.
We herein review the evidence extracted from updated literature concerning the data related to pathogenetic mechanisms and pathophysiology as well as the management of this interesting syndrome.
Keywords: Rhabdomyolysis, acute renal failure, myoglobin, crush syndrome
The first case of the crush syndrome, which constitutes one of the main causes of rhabdomyolysis, was reported in Sicily in 1908, after an earthquake1,2. In 1930, in the Baltic area, an epidemic of myoglobinuria was observed due to consumption of contaminated fish. Interest in rhabdomyolysis and crash syndrome was stimulated during the World War II particularly after the bombing in London, where the victims developed acute renal failure and myoglobinuria1.
Rhabdomyolysis is a rupture (lysis) of skeletal muscles due to drugs, toxins, inherited disorders, infections, trauma and compression3. Lysis of muscle cells releases toxic intracellular components in the systemic circulation which leads to electrolyte disturbances, hypovolemia, metabolic acidocis, coagulation defects and acute renal failure due to myoglobin4.
The skeletal muscle consists of cylindrical myofibrils, which contain variant structural and contraction proteins. Actin and myosin, arranged in thin and thick filaments respectively, form the repeated functional units of contraction, the sarcomeres5. The sarcoplasmic reticulum constitutes an important cellular calcium storage. It is structurally connected to the t-tubules, that are formed by invaginations of the muscle cell plasma membrane, the sarcelemma, around every fibril (Figure 1). After the sarcelemma depolarization, the stimulation arrives, through the t-tubules junctions, at the sarcoplasmic reticulum, inducing the calcium ions release and triggering muscle contraction6.</span>
