Rutin Improves Cardiac and Erythrocyte Membrane-Bound ATPase Activities in Male Rats Exposed to Cadmium Chloride and Lead Acetate.

Cardiovascular diseases have been associated with cadmium (Cd) and lead (Pb). Impaired Ca2+ and Na+/K+-ATPase activities have also been linked to hemolytic and cardiovascular disorders. This study investigated the effect of rutin on Cd and/or Pb-induced cardiac and erythrocyte disorders in male rats. Twenty-five (25) male Wistar rats were treated as (n=5): Control, Pb (60 mg/kg, p.o), Cd (5 mg/kg, p.o), Pb + Cd, Rutin + Pb + Cd (50 mg/kg Rt, 60 mg/kg Pb, 5 mg/kg Cd, p.o). Plasma electrolyte and Ca2+- and Na+/K+-ATPase activities in the erythrocyte and heart of the rats were assayed. There was an increased and decreased activity of cardiac and erythrocyte Na+/K+-ATPase in Pb- (172%) and Cd- (33.7%) treated groups, respectively. However, rutin increased erythrocyte Na+/K+-ATPase activity in Cd + Pb when compared with Cd and Cd + Pb groups. Erythrocyte Ca2+-ATPase activity was decreased in the Pb (68%), Cd (68%) and Cd + Pb (55.3%) groups. Cardiac Na+/K+-ATPase activity was not altered in Pb and Cd groups while it decreased in Cd + Pb. Rutin increased the activity of the pump in Cd +Pb-treated rats compared to the Cd+Pb group. Therefore, rutin reversed cadmium- and lead-induced impaired cardiac and erythrocyte membrane Ca2+- and Na+/K+-ATPase activities. Graphical Abstract Dotted lines-decrease activity, curved lines-increased activity (created with BioRender.com ).

Cysteamine mitigates torsion/detorsion-induced reperfusion injury via inhibition of apoptosis, oxidative stress and inflammatory responses in experimental rat model.

Oxidative stress, inflammation and apoptosis are major pathways in pathophysiology of testicular torsion/detorsion (TTDT) reperfusion injury. This study evaluated the antioxidant, anti-inflammatory and anti-apoptotic role of cysteamine in TTDT-induced injury. Male Wistar rats (n = 32) were grouped into four (n = 8): sham, ischaemia-reperfusion injury (IRI), cysteamine (100 mg/kg and 200 mg/kg) for in vivo study. Samples were taken for biomolecular and histological evaluation 48 hr after detorsion. Tissue SOD, GPx, GSH, GST activity, total thiol, H2 O2 and MDA were assessed. Serum levels of NO, MPO, TNF-alpha and IL-6 and sperm motility, count and viability were assessed. Caspase-3 and bax were evaluated by immunohistochemistry. Significant difference was set as p < .05. Significant increase in H2 O2, MDA and nitrite but reduction in SOD, GPx, GSH, GST and total thiol in the testicular tissue of IRI rats was reversed by cysteamine. Serum MPO and TNF-α were significantly elevated in RI, while treated-RI rats showed decrease (p < .05) in tissue level of the inflammation markers. Reduced sperm motility in RI was significantly reversed by cysteamine. Increased tissue expression of bax and caspase-3 was reversed by cysteamine. Cysteamine protected the testis against reperfusion injury through anti-inflammatory, antioxidant effects and inhibition of apoptosis in rats.

Watermelon rind ethanol extract exhibits hepato-renal protection against lead induced-impaired antioxidant defenses in male Wistar rats.

Lead acetate associated tissue injury has been linked to altered antioxidant defenses, hyperuricemia and inflammation. We hypothesized that watermelon rind extract, would ameliorate lead acetate-induced hepato-renal injury. Thirty Male Wistar rats received distilled water, lead acetate (Pb; 5 mg/kg) with or without watermelon rind extract (WM; 400 mg/kg; WM + Pb; 15 days of WM pretreatment); Pb + WM (15 days of WM post treatment) and simultaneous treatment (WM-Pb) for 30 days. Lead toxicity led to elevated serum malondialdehyde, creatinine, urea, uric acid, lactate dehydrogenase, liver injury enzymes, as well as decreased body weight. Decreased serum levels of reduced glutathione, nitric oxide, total protein and glutathione peroxidase activity was also observed. However, these alterations were ameliorated by watermelon rind extract in lead acetate-treated rats. Watermelon rind ethanol extract protects against lead acetate-induced hepato-renal injury through improved antioxidant defenses at least in part, via uric acid/nitric oxide-dependent pathway signifying the health benefits of this agricultural waste and a potential for waste recycling while limiting environmental pollution.

Rutin prevents cardiac oxidative stress and inflammation induced by bisphenol A and dibutyl phthalate exposure via NRF-2/NF-κB pathway.

AIM: Environmental pollutants such as plastic-component substances (phthalates and bisphenol A) that coexist in natural ecosystems have been linked to an increase in the occurrence of human health hazards, particularly cardiovascular health. This study was designed to investigate single and combined cardio-toxic effects of dibutyl phthalate and bisphenol-A and the possible interventional role of rutin. MATERIALS AND METHODS: Forty-two rats were randomized into 7 groups of 6 animals each and were treated as follows for 28 days: Control (0.1% DMSO), Bisphenol-A (BPA, 25 mg/kg, p.o), Dibutyl phthalate (DBP, 25 mg/kg, p.o), BPA + Rutin (25 mg/kg, Rt 50 mg/kg), DBP + Rt (25 mg/kg, Rt 50 mg/kg), BPA + DBP, BPA + DBP + Rt. Cardiac lipid peroxidation, antioxidants and inflammatory markers activities were measured. KEY FINDINGS: The result showed that BPA reduced the superoxide dismutase (SOD) activity, DBP and DBP+ BPA reduced the catalase (CAT) activity, DBP reduced glutathione (GSH) and nuclear factor erythroid 2-related factor 2 (Nrf2) while malondialdehyde (MDA) increased in DBP + BPA group. Also, DBP increased tissue C-reactive protein (CRP); DBP, DBP + BPA increased tissue nuclear factor kappa B (NF-κB); DBP + BPA increased plasma CRP; BPA increased plasma NF-κB. However, rutin efficiently reduced MDA level, CRP and NF-κB; increasing SOD, GSH and Nrf2 levels in DBP and BPA exposed rats. SIGNIFICANCE: These results revealed that bisphenol and dibutyl phthalate exposure caused oxidative stress and inflammation in the heart through Nrf2/NF-κB signaling pathway while oral administration of rutin prevents these effects via upregulation of Nrf2 and suppression of NF-κB signaling pathway.

Cadmium exposure induces cardiac glucometabolic dysregulation and lipid accumulation independent of pyruvate dehydrogenase activity.

CONTEXT: Suppressed glucose metabolism, elevated fatty acid metabolism and lipid deposition within myocardial cells are the key pathological features of diabetic cardiomyopathy. Studies have associated cadmium exposure with metabolic disturbances. OBJECTIVE: To examine the effects of cadmium exposure on cardiac glucose homeostasis and lipid accumulation in male Wistar rats. METHODS: Male Wistar rats were treated for 21 days as (n = 5): Control, cadmium chloride Cd5 (5 mg/kg, p.o.), cadmium chloride Cd30 (30 mg/kg, p.o). RESULTS: The fasting serum insulin level in this study decreased significantly. Pyruvate and hexokinase activity reduced significantly in the Cd5 group while no significant change in lactate and glycogen levels. The activity of pyruvate dehydrogenase enzyme significantly increased with an increasing dosage of cadmium. The free fatty acid, total cholesterol and triglyceride levels in the heart increased significantly with increasing dosage of cadmium when compared with the control. Lipoprotein lipase activity in the heart showed no difference in the Cd5 group but a reduction in the activity in the Cd30 group was observed. CONCLUSION: This study indicates that cadmium exposure interferes with cardiac substrate handling resulting in impaired glucometabolic regulation and lipid accumulation which could reduce cardiac efficiency.

The effect of ginger (Zingiber officinale) feed on cardiac biomarker in medium-dose isoproterenol-induced myocardial toxicity.

OBJECTIVE: Traditional medicines have been widely used to prevent and treat diseases for thousands of years. This study was designed to evaluate the effect of ginger feed on cardiac biomarker in isoproterenol (ISO)-induced myocardial toxicity. MATERIALS AND METHODS: Thirty male Wistar rats were grouped into six groups of five: Control; ISO-induced toxicity; ginger fed; ginger fed before; ginger fed+ ISO simultaneously and ginger fed after. Freshly prepared solution of ISO was injected through intraperitoneal route at a dosage of 20 mg/kg, while the control received distilled water. Blood was collected via cardiac puncture after two weeks of administration, the serum was used to evaluate biomarkers. RESULTS: The CK-MB and CK of ginger-fed groups were significantly lower compared to ISO group- 8.2±0.5 U/L and 39.36±5.28 U/L respectively, P <0.05. The CK-MB and CK levels of all ginger-fed groups showed no significant difference compared to the control- 2.2±0.3 U/L and 17. 07±3.4.90 U/L, respectively p>0.05, except ginger fed after group where they were significantly higher compared to the control. The mean value of LDH in all ginger-fed groups was lower than the ISO group (67.17±0.88 U/L; p<0.05), but significantly higher (p<0.05) than the control (26.45±2.52 U/L). The mean value of ALT in all ginger fed groups was lower than the ISO group (83.11±4.88U/L; p≤0.05). CONCLUSION: Ginger feed hindered toxic effects of isoproterenol.