t-BHQ Protects Against Oxidative Damage and Maintains the Antioxidant Response in Malnourished Rats

Abstract

Objective: Tert-butylhydroquinone (t-BHQ) protective effect against oxidative damage in thymus from malnourished pops-rats was evaluated.

Methods: Malnutrition in pops-rats was induced during the lactation period and first-, second-, and third-degree malnourished rats were studied (MN1, MN2, and MN3). To determine t-BHQ protective effect, lipid peroxidation (LPx) was assessed, as well as the carbonyl content. The reduced glutathione and glutathione disulfide content were determined and antioxidant enzyme activities were measured.

Results: Oxidative protein damage, LPx, and Nuclear Factor-κB (NF-κB) content, increased in the MN2 and MN3 compared to well-nourished rats, associated with lower protein content and antioxidant activity of superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase. Tert-butylhydroquinone treatment induced a protective effect against lipids and proteins oxidative damage, as well as decrease in NF-κB in MN rats and restored the antioxidant mechanisms, mostly GPx and SOD. No differences were found between male and female animals.

Conclusions: Results show that higher body weight deficit leads to increased oxidative damage and probably inflammation, attributable to alterations in antioxidant mechanisms. These effects were reversed by the t-BHQ-treatment, which restores the antioxidant response. Our findings suggest that t-BHQ could be an interesting pharmacological intervention, but it needs to be studied further.

Keywords: NF-κB; antioxidants; malnutrition; oxidative stress; t-BHQ.

Figure 1.

Thymus redox status in WN and MN rats treated with different t-BHQ doses 25, 50, and 75 mg t-BHQ/kg body weight. Bars represent the mean ± SE. *P < .05 significant differences between MN groups with different treatments in relation to their WN group. ^‡ P < .05 statistical differences between treated groups with (75 mg t-BHQ) in relative to corresponding NT-MN group. NT indicates nontreated; SE, standard error; t-BHQ, tert-butylhydroquinone.

Figure 2.

Lipid peroxidation and protein oxidation obtained from t-BHQ and NT, WN, and MN rats. A, Lipid peroxidation. B, Protein oxidative damage, densitometric analysis. C, Representative Oxyblot; actin was used as an internal control. Each point represents the mean ± SE. *P < .05 statistical significance between MN-t-BHQ groups in relation to their MN-NT group. ^‡ P < .05 statistical differences between MN-NT groups versus WN-NT. NT indicates nontreated; SE, standard error; t-BHQ, tert-butylhydroquinone.

Figure 3.

Antioxidant enzymes, NF-κB p50 and p65 subunits. Representative blots performed for (A) SOD, (B) GPx, (C) CAT, (D) p50, and (E) p65. Relative optic density was normalized against WN-t-BHQ or WN-NT. Each point represents the mean ± SE. *P < .05 statistical significance between MN-t-BHQ in relation to their MN-NT group. ^‡ P < .05 significant differences between MN-NT groups (black line) or MN-t-BHQ (dotted line) with respect to their WN. GPx indicates glutathione peroxidase; NT, nontreated; SE, standard error; SOD, superoxide dismutase; t-BHQ, tert-butylhydroquinone.

Figure 4.

Figure shows the enzymatic activity for (A) SOD, (B) GPx, and (C) CAT. Each point represents the mean ± SE. *P < .05 statistical significance between MN-t-BHQ groups in relation to their MN-NT group. ^‡ P < .05 significant differences between MN-NT groups (black line) or MN-t-BHQ (dotted line) with respect to their WN. GPx indicates glutathione peroxidase; NT, nontreated; SE, standard error; SOD, superoxide dismutase; t-BHQ, tert-butylhydroquinone.