Study summary · research use only
L-glutathione 1% promotes neuroprotection of nitrergic neurons and reduces the oxidative stress in the jejunum of rats with Walker-256-bearing tumor
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This rat study examined the effects of L-glutathione (1%) treatment in Walker-256 tumor-bearing rats, using four groups: control, control treated with L-glutathione, tumor-bearing, and tumor-bearing treated with L-glutathione. After 14 days of tumor inoculation, jejunum tissue was analyzed for nitrergic (nNOS-immunoreactive) neurons and 3-Nitrotyrosine, alongside oxidative stress and inflammatory markers in tissue and plasma. Tumor-bearing rats showed decreased reduced glutathione, which was prevented by L-glutathione treatment, along with increased lipoperoxidation and plasma malondialdehyde that L-glutathione treatment did not prevent. Total antioxidant capacity was altered in both tumor-bearing groups, with a better plasma index in the treated group; IL-10 and TNF-α increased with treatment. The density of nNOS-immunoreactive neurons decreased in tumor-bearing rats' jejunum myenteric plexus, an effect prevented by L-glutathione treatment.
Abstract
Our main goals were to investigate the effects of L-glutathione (1%) treatment in Walker-256 tumor-bearing rats by analyzing immunoreactive neurons (IR), responsive to the nNOS enzyme and 3-Nitrotyrosine, in their jejunum myenteric plexus. Moreover, the oxidative state and inflammatory process in these animals were investigated. Four experimental groups were utilized: control (C), control treated with L-glutathione (CGT), Walker-256 tumor-bearing rats (TW), and Walker-256 tumor-bearing rats treated with L-glutathione (TWGT). After 14 days of tumor inoculation, the jejunum was collected for immunohistochemical techniques and assessment of oxidative status. Plasma was collected to evaluate oxidative status and measure cytokines. The TW group exhibited a decrease of reduced glutathione in their jejunum, which was prevented in the L-glutathione treated TWGT group. TW animals presented pronounced oxidative stress by increasing levels of lipoperoxidation in their jejunum and malondialdehyde in their plasma; however, the L-glutathione treatment in TWGT group was not able to avoid it. The total antioxidant capacity was altered in groups TW and TWGT, yet the last one had a better index in their plasma. The IL-10, and TNF-α levels increased in TWGT animals. The nNOS-IR neuron density decreased in the jejunum myenteric plexus of the TW group, which was avoided in the TWGT group. The nNOS +3-Nitrotyrosine neurons quantification did not show significative alterations. The treatment with L-glutathione (1%) imposed an important defense to some parameters of oxidative stress induced by TW-256, leading to neuroprotection to the loss in the nNOS-IR neuron density.
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