After death, several physiological and biochemical processes occur that lead to muscle cells being unable to prevent calcium ion (Ca²⁺) entry. Here are the main factors contributing to this phenomenon:
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Loss of Membrane Integrity: Upon death, cells begin to lose their structural integrity. The cell membranes become more permeable, allowing ions, including calcium, to enter the cytoplasm from the extracellular space.
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Depletion of ATP: Muscle contraction and relaxation are regulated by adenosine triphosphate (ATP). After death, ATP production ceases because metabolic processes stop. ATP is essential for the function of calcium pumps (such as the sarcoplasmic reticulum calcium ATPase, SERCA) that normally help to remove Ca²⁺ from the cytoplasm and maintain low levels of calcium.
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Failure of Calcium Pumps: Without ATP, the calcium transport mechanisms in muscle cells fail. The sarcoplasmic reticulum, which stores calcium, can’t pump calcium back into its lumen, leading to increased cytosolic calcium levels.
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Calcium Leakage: With the integrity of the sarcoplasmic reticulum compromised and ion gradients disrupted, calcium can leak into the cytoplasm uncontrollably, further increasing cellular calcium levels.
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Postmortem Changes: These events lead to a state called "rigor mortis," where calcium enters the muscle cells, causing sustained contraction because the actin and myosin filaments in muscle fibers interact in the absence of sufficient ATP to release them.
In summary, after death, the combination of membrane breakdown, ATP depletion, and the failure of ion transport mechanisms leads to increased calcium concentrations in muscle cells, ultimately preventing the prevention of calcium ion entry and resulting in the rigid state characteristic of rigor mortis.