Match the columns.
| Column-A (Disorder) | Column-B (Enzyme) |
| i. Gaucher disease | a. Phenylalanine hydroxylase |
| ii. Hunter syndrome | b. Hexosaminidase A |
| iii. Tay-Sachs disease | c. Iduronate-2-sulfatase |
| iv. Phenylketonuria | d. Glucocerebrosidase |
Show answer & explanation
Correct answer: C
Explanation
The correct answer is option 3 i.e. i-d, ii-c, iii-b, iv-a.
- Gaucher disease (i) is linked to glucocerebrosidase (d), as its deficiency causes harmful lipid buildup.
- Hunter syndrome (ii) results from a lack of iduronate-2-sulfatase (c), leading to glycosaminoglycan accumulation.
- Tay-Sachs disease (iii) stems from hexosaminidase A (b) deficiency, causing GM2 ganglioside storage in neurons.
- Phenylketonuria (iv) arises due to defective phenylalanine hydroxylase (a), increasing phenylalanine levels and causing neurological damage.
These enzyme deficiencies disrupt metabolic pathways, leading to severe genetic disorders. Gaucher and Tay-Sachs involve lipid metabolism, Hunter syndrome affects carbohydrate breakdown, and phenylketonuria impairs amino acid processing. Early diagnosis and enzyme replacement therapies can manage some conditions, but prevention through genetic screening remains critical.