Does l-glutamine-supplemented diet extenuate NO-mediated damage on myenteric plexus of Walker 256 tumor-bearing rats?

- Enteric innervation damage was demonstrated in cancer cachexia rat model.
- Cachectic rats showed high lipid peroxidation and NO levels in jejunum samples.
- Enteric neuropathy was partially prevented by l-glutamine-supplemented diet.
- The higher nNOS expression was prevented by l-glutamine in the ileum exclusively.

This study was designed to appraise the relationship between enteric neuropathy and oxidative stress in cancer cachexia under l-glutamine-supplemented diet. Total and nitrergic neuronal populations were investigated in jejunum and ileum in four experimental groups: control (C); control l-glutamine-supplemented diet (CG); Walker-256 tumor (TW); and Walker-256 tumor supplemented with l-glutamine (TWG). In addition, local oxidative stress, neuronal nitric oxide synthase (nNOS) enzyme and nitric oxide (NO) levels were evaluated. Neuronal density and somatic area of the total and nitrergic populations were reduced in TW rats, which was accompanied by high oxidative stress, NO and nNOS levels. l-glutamine supplementation prevented neuronal atrophy, changes in pan neuronal density and nNOS overexpression (ileum), and restored total antioxidant capacity. Nevertheless, the oxidative stress was partially mitigated and no effect was observed on the reduction of nitrergic population and NO levels. l-glutamine-supplemented diet extenuates NO-mediated damage on the myenteric plexus although has a small benefit on oxidative stress.

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