Question

After giving her dog a bath, a young girl suddenly died. The flea dip she was using on the dog contains a chemical called rotenone which inhibits the function of an enzyme that oxidizes NADH to NAD+. Her autopsy revealed massive cell death in her internal organs and damage to her mitochondria. The levels of NAD+ were very low and the levels of NADH were very high in her mitochondria. What part of cellular respiration was affected by the rotenone (1 pt)? How could this have led to her death (1 pt)?

Answer 1

In spite of the fact that this situation is probably not going to occur, rotenone is poisonous in light of the fact that it meddles with the electron transport chain (ETC) in mitochondria, so NADH would develop as recommended.

Answer 2

Ans.

The rotenone is toxic chemical, which targets electron transport chain of cellular respiration, during which NADH are oxidized to NAD+ provide energy for ATP synthesis. It inhibits electron transfer from complex I (iron-sulfur center) to ubiquinone.

The increased amount of NADH is increased in girl's cell as NADH does not get oxidized into NAD+, due to rotenone. As electron transport provides energy for ATP synthesis, inhibition of electron transport chain results in no ATP synthesis.

ATP molecules act as energy-providing molecules for all cellular activities. So, lack of ATP molecules results in death as cells lack energy to perform biological functions.

Thus, the part of girl's cellular respiration, affected by rotenone was electron transport chain and her death was caused due to inhibition of ATP synthesis.