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This research investigates the requirement of l-arginine for the activation of macrophage cytotoxic mechanisms that inhibit target cell metabolism.

January 1, 1987The Journal of ImmunologyOpen Access

L-arginine is required for expression of the activated macrophage effector mechanism causing selective metabolic inhibition in target cells.

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Randomized trial demonstrates l-arginine's role in macrophage cytotoxic effects in target cells, suggesting metabolic inhibition mechanisms.

This research investigates the requirement of l-arginine for the activation of macrophage cytotoxic mechanisms that inhibit target cell metabolism.
Examined the effect of l-arginine on mitochondrial respiration and DNA synthesis in target cells.
Assessed the impact of analogues and inhibitors on the l-arginine-dependent effector mechanism.
Determined the role of lipopolysaccharide in conjunction with l-arginine in activating cytotoxic macrophages.
Inhibition of mitochondrial respiration in target cells is proportional to l-arginine concentration (effect seen in the presence of l-arginine).
NG-monomethyl-l-arginine is a competitive inhibitor of the effector mechanism, but elevated l-arginine can override its effects.
Bacterial lipopolysaccharide requires l-arginine for effectiveness and does not alleviate inhibition caused by NG-monomethyl-l-arginine.

Hibbs et al. (1987) studied this question.

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January 1, 1987The Journal of ImmunologyOpen Access

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Authors

Randomized trial demonstrates l-arginine's role in macrophage cytotoxic effects in target cells, suggesting metabolic inhibition mechanisms.

This research investigates the requirement of l-arginine for the activation of macrophage cytotoxic mechanisms that inhibit target cell metabolism.
Examined the effect of l-arginine on mitochondrial respiration and DNA synthesis in target cells.
Assessed the impact of analogues and inhibitors on the l-arginine-dependent effector mechanism.
Determined the role of lipopolysaccharide in conjunction with l-arginine in activating cytotoxic macrophages.
Inhibition of mitochondrial respiration in target cells is proportional to l-arginine concentration (effect seen in the presence of l-arginine).
NG-monomethyl-l-arginine is a competitive inhibitor of the effector mechanism, but elevated l-arginine can override its effects.
Bacterial lipopolysaccharide requires l-arginine for effectiveness and does not alleviate inhibition caused by NG-monomethyl-l-arginine.

Hibbs et al. (1987) studied this question.

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