Veterinary Pharmacology and Toxicology- ICAR JRF/SRF 2024

• Ruminal Metabolism and Toxic Activation:
• Cyanogenic Glycosides (e.g., dhurrin in immature sorghum/jowar, linamarin in linseed/flax):
• Intact cyanogenic glycosides are relatively non-toxic when consumed.
• In the rumen, microbial $\beta$-glucosidase and hydroxynitrile lyase enzymes rapidly hydrolyze the glycosides, liberating free, lethal Hydrocyanic Acid (HCN / Cyanide):

• Free cyanide binds ferric iron ($Fe^{3+}$) in cytochrome oxidase, arresting cellular respiration. Hence, ruminal metabolism directly intensifies its toxicity.
• nalysis:
• (Cyanogenic glycosides): Correct.

Correct option: (3) Cyanogenic glycosides

• Pathogenesis of Secondary Photosensitization:
• Assertion (A): Photosensitization is a photodynamic reaction wherein an absorbing molecule in cutaneous capillaries is activated by UV/sunlight ($320 - 400\text{ nm}$), producing reactive oxygen species that induce severe cutaneous necrosis and dermatitis. (True).
• Reason (R): In ruminants, Phylloerythrin is a porphyrin breakdown product of chlorophyll produced by rumen microbes and normally excreted in bile. Diffuse liver injury (facial eczema from sporidesmin, lantana toxicity, pyrrolizidine alkaloids) impairs biliary excretion, causing phylloerythrin to spill into dermal blood circulation where sunlight activates it. (True).
• nalysis:
• Both (A) and (R) are true, and (R) is the precise physiological cause of (A). Hence, Option 1 is correct.

• Biosynthesis of Endogenous Nitric Oxide (NO):
• Nitric oxide is an endothelial-derived relaxing factor (EDRF) synthesized by the family of Nitric Oxide Synthase (NOS) enzymes (eNOS, nNOS, iNOS).
• The reaction requires molecular oxygen, NADPH, and tetrahydrobiopterin ($BH_4$), using L-Arginine as the obligatory amino acid substrate:

• nalysis:
• (Arginine): Correct primary substrate.

Correct option: (4) Arginine