Longterm melatonin administration alleviates paraquat mediated oxidative stress in Drosophila melanogaster.

We investigated the effect of melatonin (MEL) in the activities of cytosolic superoxide dismutase (SOD) and catalase as well as in the levels of H2O2 and mitochondrial malondialdehyde (MDA) in paraquat-intoxicated Drosophila melanogaster. Paraquat (40 mM) was administrated for 36 h. Three groups of flies intoxicated with paraquat were used: PQ (exposed during 36h to paraquat), PQ-MEL (exposed during 36h to paraquat and then treated with MEL [0.

Effects of melatonin on oxidative stress, and resistance to bacterial, parasitic, and viral infections: a review.

Melatonin, a hormone secreted by the pineal gland, works directly and indirectly as a free radical scavenger. Its other physiological or pharmacological activities could be dependent or independent of receptors located in different cells, organs, and tissues. In addition to its role in promoting sleep and circadian rhythms regulation, it has important immunomodulatory, antioxidant, and neuroprotective effects suggesting that this indole must be considered as a therapeutic alternative against infections.

Minocycline increases the activity of superoxide dismutase and reduces the concentration of nitric oxide, hydrogen peroxide and mitochondrial malondialdehyde in manganese treated Drosophila melanogaster.

The toxicity caused by high concentrations of manganese (Mn) could be due to a production of free radicals. Minocycline is an effective antioxidant with a high potential to capture free radicals. We investigated the effect of minocycline in the activities of superoxide dismutase (SOD) and catalase, and in the concentrations of nitric oxide (NO), hydrogen peroxide (H2O2) and mitochondrial malondialdehyde (MDA) in manganese-treated Drosophila melanogaster.

Paricalcitol downregulates myocardial renin-angiotensin and fibroblast growth factor expression and attenuates cardiac hypertrophy in uremic rats.

Background: Vitamin D attenuates uremic cardiac hypertrophy, possibly by suppressing the myocardial renin-angiotensin system (RAS) and fibroblast growth factors (FGFs). We compared the suppression of cardiac hypertrophy and myocardial expression of RAS and FGF receptor genes offered by the vitamin D analog paricalcitol (Pc) or the angiotensin-converting enzyme inhibitor enalapril (E) in experimental uremia.

Methods: Rats with 5/6 nephrectomy received Pc or E for 8 weeks.

Experimental induction of salt-sensitive hypertension is associated with lymphocyte proliferative response to HSP70.

Renal tubulointerstitial inflammation is a constant feature of experimental models of hypertension and likely plays a role in the pathogenesis of salt-sensitive hypertension. We have previously raised the possibility that the immune cell infiltration is driven by a low grade autoimmune reactivity directed to or facilitated by renal heat shock protein over expression. The present studies were done to gain insight on possible cell-mediated immune mechanisms in experimental hypertension by determining the renal expression of HSP70 and the proliferation index of T lymphocytes cultured with HSP70.

Suppression of renin-angiotensin gene expression in the kidney by paricalcitol.

The renal renin-angiotensin system plays a major role in determining the rate of chronic renal disease progression. Treatment with activators of the vitamin D receptor retards the progression of experimental chronic renal disease, and vitamin D is known to suppress the renin-angiotensin system in other organs. Here we determined if the beneficial effects of paricalcitol (19-nor 1,25-dihydroxyvitamin D(2)) were associated with suppression of renin-angiotensin gene expression in the kidney.

Mycophenolate mofetil administration reduces renal inflammation, oxidative stress, and arterial pressure in rats with lead-induced hypertension.

Hypertension is a likely consequence of chronic lead exposure in humans, especially in association with reduced renal function and in high risk populations. Numerous studies have demonstrated that oxidative stress plays an important role in the pathogenesis of experimental lead-induced hypertension and we have shown recently that tubulointerstitial immune cell infiltration is a feature of chronic low-dose lead exposure. Since oxidative stress, renal inflammation, and angiotensin activity are closely linked characteristics in experimental models of hypertension, we decided to investigate whether lead-induced hypertension would be ameliorated by suppressing renal inflammation with the immunosuppressive drug mycophenolate mofetil (MMF).