High environmental temperature potentiated marker of oxidative cellular damage and renal expression of p38 MAPK in male rats fed a high salt diet

Abstract

Aim: Oxidative stress, heat shock protein (HSP70) and p38 mitogen-activated protein kinase (MAPK) are important functional cellular signals involved in the pathophysiology of cardiovascular diseases. This study investigated the effect of high environmental temperature (HET) and high salt diet (HSD) respectively and together on systemic oxidative stress, nitric oxide (NO), HSP70 and  renal p38 MAPK.

Methods: Thirty-two male Sprague-Dawley rats were divided into four groups with eight rats in each group: Control rats (C) fed a normal diet; salt-loaded rats (S) fed a HSD (8%NaCl); normal diet rats (H) exposed to HET (38.5 ± 0.5^oC 4h daily for 8weeks); and salt-loaded rats (SH), fed a HSD and exposed to HET. Circulatory oxidative stress parameters (SOD: superoxide dismutase; GSH: glutathione; CAT: catalase; MDA: malondialdehyde), HSP70 and renal p38 MAPK were determined by colorimetric, enzyme-linked immunosorbent assay (ELISA) methods and immunohistochemistry (IHC) techniques respectively.

Results:  Plasma GSH concentration and CAT activity decreased significantly, with significant increase in MDA concentration in all the rat groups compared to control. However, MDA in SH rats was significantly higher than in either S or H rats. Circulatory HSP70 and NO were significantly raised in S and H rats but unchanged in SH rats compared to control. Conversely, renal expression of p38 MAPK was significantly increased in H and SH rats compared to control, but SH rats had significantly higher level than either S or H rats. SH rats also had weight gain slowing compared to control.

Conclusion: Our findings indicate that prolonged exposure to HET and HSD intakes synergistically increased renal p38 MAPK and circulatory product of oxidative cellular damage without alteration in circulatory HSP70 and NO.