Search

Sodium fluoride (NaF) is one of the neglected environmental toxicants that has continued to silently cause toxicity to both humans and animals. NaF is universally present in water, soil and the atmosphere. The persistent and alarming rate of increase in cardiovascular and renal diseases and disorders caused by chemicals such as sodium fluoride (NaF) in mammalian tissues have led to the use of various drugs for the treatment of these diseases. This study aims at evaluating the renoprotective and antihypertensive effects of L- Arginine against NaF-induced nephrotoxicity. Thirty male Wistar rats (150–180 g) were used in this study. The rats were randomly divided into five groups of six rats each as Control, NaF (300 ppm), NaF + L- Arginine (100 mg/kg), NaF + L- Arginine (200 mg/kg), and NaF + Lisinopril (10 mg/kg), respectively; orally for eight days. Histopathological examination and immunohistochemistry of renal angiotensin converting enzyme (ACE) and mineralocorticoid receptor (MCR) were performed. Markers of renal damage, oxidative stress, antioxidant defence system, and blood pressure parameters were determined. L- Arginine and Lisinopril significantly (p

This study was designed to investigate the modulatory role of Luteolin (Lut) on haemodynamic parameters and the potential mechanisms involving renal Angiotensin II (AT2R) and Mineralocorticoid (MCR) receptors in renal toxicity induced by co-exposure to Diclofenac (Dcf) and sodium fluoride (NaF) in rats. Male Wistar rats were administered with either vehicle (control), Dcf only (9 mg/kg orally) or concurrently with NaF (300 ppm in drinking water). Other groups were treated with LutA (100 mg/kg) or LutB (200 mg/kg) along with Dcf and NaF exposures. All treatments lasted 8 days, following which blood pressure indices were measured using tail-cuff plethysmography. Renal expressions of AT2R and MCR were studied with immunohistochemistry, while biomarkers of oxidative and antioxidant status were also measured in the kidneys. Systolic, diastolic and mean arterial pressures were significantly (p2R and MCR was high in the Dcf and Dcf+NaF groups, treatment with Lut caused obvious reduction in the renal expression of these receptors. Increased lipid peroxidation (Malondialdehyde) and protein oxidation (protein carbonyls) with a lowering of reduced glutathione levels contributed to the renal toxicity of Dcf, which was significantly ameliorated in Lut-treated rats. The protective effect of Lut on blood pressure was probably mediated by stimulation of renal expressions of AT2R and MCR, reduction of oxidative stress and an improvement of renal antioxidant status.

Sodium fluoride (NaF) is one of the neglected environmental toxicants that has continued to silently cause toxicity to both humans and animals. NaF is universally present in water, soil and the atmosphere. The persistent and alarming rate of increase in cardiovascular and renal diseases and disorders caused by chemicals such as sodium fluoride (NaF) in mammalian tissues have led to the use of various drugs for the treatment of these diseases. This study aims at evaluating the renoprotective and antihypertensive effects of L- Arginine on NaF-induced nephrotoxicity. Thirty male Wistar rats (150 – 180 g) were used in this study. The rats were randomly divided into five groups of six rats each as Control, NaF (300 ppm), NaF + L- Arginine (100 mg/kg), NaF + L- Arginine (200 mg/kg), and NaF + Lisinopril (10 mg/kg), respectively; orally for eight days. Histopathological examination and immunohistochemistry of renal angiotensin converting enzyme (ACE) and mineralocorticoid receptor (MCR) were performed. Markers of renal damage, oxidative stress, antioxidant defence system, and blood pressure parameters were determined. L- Arginine significantly (p hydrogen peroxide (H2O2), malondialdehyde (MDA) and protein carbonyl (PCO) and concurrent increase in the levels of antioxidant enzymes in the kidney of hypertensive rats treated with L arginine. The results of this study suggest that L- Arginine normalized high blood pressure, reduced oxidative stress, reduced the expression of renal ACE and MCR, and improved nitric oxide production. Thus, L- Arginine holds promise as a potential therapy against hypertension and renal damage.