Answer:
The correct answer is C production of FAD to FADH2 by the citric acid cycle represent the energetic capacity to synthesize about 1.5 ATP.
Explanation:
Citric acid cycle is one of most important stage of cellular respiration.Citric acid cycle or TCA cycle composed of various enzyme catalyzed biochemical reaction.
various reduced coenzymes are produced during TCA cycle such as NADH,FADH2.FADH2 is formed from FAD during the conversion of succinate to fumarate.
The FADH2 then enter electron transport chain to oxidize itself into FAD along with the generation of 1.5 ATP.
The stomach<span> is a muscular hollow organ. It takes in food from the esophagus (gullet or food pipe), mixes it, breaks it down, and then passes it on to the small intestine in small portions. The entire digestive system is made up of one muscular tube extending from the mouth to the anus.
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~Isle of flightless Duns</span>
The answer is Observation. That's the first step.
Mitochondria because it releases stored food which is used for power growth and development and movement..and muscle have the greatest demand for them than any other body cell
Numerous antiepileptic medications, such phenytoin, have been designed to block voltage-gated sodium channels (VGSC) in neuronal membrane. In addition, multiple toxins and pharmacological modulators work by attaching to various biophysical states of the VGSC to cause their effects. Depending on how modulatory agents act, some VGSC states are stabilized or destabilized, altering the channel's biophysical properties. The first anticonvulsant to successfully treat epileptic disorders without causing undesirable side effects such as brain drowsiness was phenytoin.
Phenytoin has been indicated to block high-frequency neuronal activity potentials from the inner vestibule of the pore, as demonstrated by electrophysiological research and site-directed mutation.
Frequency and voltage both affect phenytoin binding.
There are theories that phenytoin interferes with the late sodium current that sustains depolarizations in epilepsy by blocking non-inactivated channels.
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