1. Fat is burned on the wick of carbohydrate
Ans: the oil in the lamp by itself cannot be lighted, the flame needs a wick
Likewise, fats are burned in the fire of carbohydrate
Fat is Acetyl CoA, Wick is Oxaloacetate
In our body oxidation of fat (acetyl CoA), needs the help of oxaloacetate.
One passage of the cycle oxidizes acetyl CoA into two CO2 molecules.
Oxaloacetate acts as a true catalyst, it enters the cycle and is regenerated in the
end.
The major source of oxaloacetate is pyruvate.
Hence carbohydrates are required for the oxidation of fat.
2. Viper snake bite leads to haemolysis.
Ans: Phospholipase A2 enzyme present in venom of viper snake
Phospholipases are the enzymes that hydrolyse phospholipids.
Phospholipase A2 acts on intact lecithin molecule hydrolysing the fatty acid
esterified second carbon atom.
The products are lysolecithin and fatty acid
Lysolecithin is a detergent and hemolytic agent
This lysolectin causes hemolysis and renal failure in snake poisoning.
3. Folic acid deficiency presents with macrocytic anemia.
, When methylene THFA gets converted to methyl THFA, one carbon group is
transferred to dUMP which is converted to dTMP by thymidylate synthase
enzyme. dTTP is required for DNA synthesis.
In case of folic acid deficiency, THFA is reduced and thymidylate synthase
enzyme is inhibited. Hence dUMP is not converted to dTMP. So dTTP is not
available for DNA synthesis.
During erythropoiesis, DNA synthesis is delayed, but protein synthesis is
continued.
Thus hemoglobin accumulates in RBC precursors.
This results in asynchrony manifesting as immature nucleus and mature
cytoplasm which leads to macrocytes.
These abnormal RBC are rapidly destroyed in spleen, this haemolysis leads to
reduced lifespan of RBC resulting in anemia.
4. LDL and Atherosclerosis
Excess LDL cholesterol, which is not processed by hepatic receptors, is
oxidized to form oxidised LDL which is taken up by monocytes and
macrophages.
Monocytes rich in oxidized LDL migrate into sub endothelial spaces and
become macrophages, these macrophages will get converted to foam cells.
Foam cells are deposited in the arterial wall below the intima to form the
earliest atherosclerosis lesion called as fatty streak which progress to
atherosclerotic plaques.
5. Methotrexate acts as an anti-cancerous drug. Reason out
Methotrexate is structurally similar to folic acid.
It competitively inhibits folate reductase. So THFA is not produced. THFA is
required for incorporation of C2 and C8 of purines and C5 methyl groups in
thymidine.
Thus methotrexate inhibits DNA synthesis and thereby inhibiting cell division.
Therefore, methotrexate is used as a anti-cancerous drug. Eg in treatment of
choriocarcinoma and acute leukemias,etc.
Ans: the oil in the lamp by itself cannot be lighted, the flame needs a wick
Likewise, fats are burned in the fire of carbohydrate
Fat is Acetyl CoA, Wick is Oxaloacetate
In our body oxidation of fat (acetyl CoA), needs the help of oxaloacetate.
One passage of the cycle oxidizes acetyl CoA into two CO2 molecules.
Oxaloacetate acts as a true catalyst, it enters the cycle and is regenerated in the
end.
The major source of oxaloacetate is pyruvate.
Hence carbohydrates are required for the oxidation of fat.
2. Viper snake bite leads to haemolysis.
Ans: Phospholipase A2 enzyme present in venom of viper snake
Phospholipases are the enzymes that hydrolyse phospholipids.
Phospholipase A2 acts on intact lecithin molecule hydrolysing the fatty acid
esterified second carbon atom.
The products are lysolecithin and fatty acid
Lysolecithin is a detergent and hemolytic agent
This lysolectin causes hemolysis and renal failure in snake poisoning.
3. Folic acid deficiency presents with macrocytic anemia.
, When methylene THFA gets converted to methyl THFA, one carbon group is
transferred to dUMP which is converted to dTMP by thymidylate synthase
enzyme. dTTP is required for DNA synthesis.
In case of folic acid deficiency, THFA is reduced and thymidylate synthase
enzyme is inhibited. Hence dUMP is not converted to dTMP. So dTTP is not
available for DNA synthesis.
During erythropoiesis, DNA synthesis is delayed, but protein synthesis is
continued.
Thus hemoglobin accumulates in RBC precursors.
This results in asynchrony manifesting as immature nucleus and mature
cytoplasm which leads to macrocytes.
These abnormal RBC are rapidly destroyed in spleen, this haemolysis leads to
reduced lifespan of RBC resulting in anemia.
4. LDL and Atherosclerosis
Excess LDL cholesterol, which is not processed by hepatic receptors, is
oxidized to form oxidised LDL which is taken up by monocytes and
macrophages.
Monocytes rich in oxidized LDL migrate into sub endothelial spaces and
become macrophages, these macrophages will get converted to foam cells.
Foam cells are deposited in the arterial wall below the intima to form the
earliest atherosclerosis lesion called as fatty streak which progress to
atherosclerotic plaques.
5. Methotrexate acts as an anti-cancerous drug. Reason out
Methotrexate is structurally similar to folic acid.
It competitively inhibits folate reductase. So THFA is not produced. THFA is
required for incorporation of C2 and C8 of purines and C5 methyl groups in
thymidine.
Thus methotrexate inhibits DNA synthesis and thereby inhibiting cell division.
Therefore, methotrexate is used as a anti-cancerous drug. Eg in treatment of
choriocarcinoma and acute leukemias,etc.
