Recall that in the Hardy-Weinberg lab we did earlier in the semester, the clams in some of the populations we studied were exposed to saxitoxin. Some of these clams were sensitive to the toxin. Saxitoxin affected the sensitive clams by blocking their voltage-gated sodium channels, ultimately killing the clams. Now that you know more about the role of voltage-gated sodium channels from completing this lab, explain why the saxitoxin killed those clams.

Question

Nick Edwards

Biology

17 October, 09:14

Recall that in the Hardy-Weinberg lab we did earlier in the semester, the clams in some of the populations we studied were exposed to saxitoxin. Some of these clams were sensitive to the toxin. Saxitoxin affected the sensitive clams by blocking their voltage-gated sodium channels, ultimately killing the clams. Now that you know more about the role of voltage-gated sodium channels from completing this lab, explain why the saxitoxin killed those clams.

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Answers (1)

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Lexi Stuart · Answer 1

Due to failure of vital organ system and body functions

Explanation:

Saxitoxin is a toxin that acts as a blocker to the voltage-gated sodium channels. It binds to voltage-gated sodium channels within the muscle and the nerve fibers and causes Paralytic Shellfish Poisoning following bioaccumulation and ingestion. It binds to the receptor at the voltage gate and causes inward Na + flow thereby substituting cation. Its high exposure could lead to muscle paralysis and respiratory failure leading to death of clams