Postmortem hypoxanthine levels in the vitreous humor are useful for estimating time since death because hypoxanthine:
- A Is produced by hepatic glycogenolysis and diffuses into vitreous
- B Is synthesised de novo in the vitreous by retinal cells during decomposition
- C Reflects antemortem ischaemia and does not change after death
- D Accumulates from ATP degradation as adenine nucleotides break down after cell death ✓
Explanation
After death, ATP is progressively degraded through ADP → AMP → IMP → inosine → hypoxanthine. Vitreous hypoxanthine accumulates in a time-dependent manner and has been proposed as a biochemical marker of PMI. Its concentration rises continuously after death, making it a complement to vitreous potassium. It does not originate from hepatic metabolism or de novo retinal synthesis.
Reference: The Essentials of Forensic Medicine and Toxicology (Narayan Reddy), 34th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.