<p>The present study investigated the effects of heat on redox balance in rat plasma and liver after 28&#xa0;days of exposure. Twenty-four Wistar rats (140–150&#xa0;g) were assigned into four (4) groups: non-heat-exposed (control), heat-exposed, heat-recovery (7&#xa0;days of recovery post-exposure), and vitamin C (50&#xa0;mg/kg bw) + heat-exposed. Compared with the control group, the animals exposed to heat exhibited a decrease in the levels of total protein and antioxidant markers (reduced glutathione, superoxide dismutase activity, nuclear erythroid factor 2-related factor-2 level (Nrf2), and catalase) in the rat plasma and liver. Furthermore, levels of oxidative stress markers (DNA fragmentation, malondialdehyde, and nitric oxide) increased appreciably in the heat-exposed rats, as did the levels of plasma alanine transaminase, acetylcholine esterase, and cortisol. On the other hand, the heat-recovery group had significantly lower levels of DNA fragmentation and cortisol than the heat-exposed group. Meanwhile, the administration of vitamin C improved the biochemical alterations caused by heat exposure; there was an appreciable elevation in the levels of antioxidant molecules and a corresponding decrease in the level of stress markers. The liver histopathology showed no signs of acute or chronic damage across all treatment groups. Collectively, the data showed that heat exposure adversely affected redox balance, causing oxidative stress and raising cortisol levels in rats. However, vitamin C + heat-exposed and/or recovery groups had improved biochemical indices, suggesting the effects of heat exposure might be reversible. In addition, data suggest that the use of antioxidants like vitamin C could ameliorate heat-induced stress and related conditions.</p>

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Vitamin C mitigates thermal stress–induced oxidative imbalance and cortisol elevation in Wistar rats

  • Damilare Emmanuel Rotimi,
  • Adeola Aminat Ajibola,
  • Gibson Ifeanyi Okonkwo,
  • Oluyomi Stephen Adeyemi

摘要

The present study investigated the effects of heat on redox balance in rat plasma and liver after 28 days of exposure. Twenty-four Wistar rats (140–150 g) were assigned into four (4) groups: non-heat-exposed (control), heat-exposed, heat-recovery (7 days of recovery post-exposure), and vitamin C (50 mg/kg bw) + heat-exposed. Compared with the control group, the animals exposed to heat exhibited a decrease in the levels of total protein and antioxidant markers (reduced glutathione, superoxide dismutase activity, nuclear erythroid factor 2-related factor-2 level (Nrf2), and catalase) in the rat plasma and liver. Furthermore, levels of oxidative stress markers (DNA fragmentation, malondialdehyde, and nitric oxide) increased appreciably in the heat-exposed rats, as did the levels of plasma alanine transaminase, acetylcholine esterase, and cortisol. On the other hand, the heat-recovery group had significantly lower levels of DNA fragmentation and cortisol than the heat-exposed group. Meanwhile, the administration of vitamin C improved the biochemical alterations caused by heat exposure; there was an appreciable elevation in the levels of antioxidant molecules and a corresponding decrease in the level of stress markers. The liver histopathology showed no signs of acute or chronic damage across all treatment groups. Collectively, the data showed that heat exposure adversely affected redox balance, causing oxidative stress and raising cortisol levels in rats. However, vitamin C + heat-exposed and/or recovery groups had improved biochemical indices, suggesting the effects of heat exposure might be reversible. In addition, data suggest that the use of antioxidants like vitamin C could ameliorate heat-induced stress and related conditions.