Abstract:Mercury exposure induces endothelial dysfunction leading to loss of endothelium-dependent vasorelaxation due to decreased nitric oxide (NO) bioavailability via increased oxidative stress. Our aim was to investigate whether acute treatment with methyl mercury chloride changes the endothelium-dependent vasodilator response and to explore the possible mechanisms behind the observed effects. Wistar rats were treated with methyl mercury chloride (5 mg/kg, po.). The methyl mercury chloride treatment resulted in an i… Show more
“…In the present study, the Merc administration caused an increase in NO level of renal tissue, which is in agreement with other studies ( 26 ). NO increasing results in a cascade reaction and then free radicals' production.…”
Background and purpose:
Mercuric chloride (Merc) can cause kidney toxicity. Harmine (Harm), an herbal alkaloid has various pharmacological and medicinal effects mainly because of its antioxidant activity. In this study, therefore, Harm's protective mechanisms on Merc-induced nephrotoxicity in BALB/c male mice were investigated.
Experimental approach:
Forty-eight male mice were randomly divided into six groups (n = 8). Groups were received saline, Merc (0.5 mL/day of 0.5 ppm aqueous), Harm (5, 10, 15 mg/kg/day), Merc + Harm (5, 10, 15 mg/kg/day) for 14 consecutive days. Saline and Harm were administrated intraperitoneally and Merc dissolved in drinking water. Urea and creatinine serum levels, body weight, kidney weight, quantitative and qualitative histological alterations, apoptosis rate, total antioxidant capacity (TAC), superoxide dismutase (SOD), and nitric oxide (NO) levels were evaluated.
Findings/Results:
There was a significant reduction in total body and kidney weights, renal histological criteria, TAC, SOD levels in the Merc group compared to the control group (
P
< 0.05), whereas these parameters in the Merc + Harm groups, were significantly increased compared to the Merc group (
P
< 0.05). Urea and creatinine serum levels, levels of NO, and apoptosis were significantly higher in the Merc group than the control, while these parameters were decreased in the Merc + Harms groups in comparison with the Merc group (
P
< 0.05).
Conclusion and implications:
Harm protected Merc-induced renal damage in mice. This protection was observed in both histological and biochemical respects. The beneficial effect of Harm was related to its antioxidant properties that diminish NO production and apoptosis induction in the kidney.
“…In the present study, the Merc administration caused an increase in NO level of renal tissue, which is in agreement with other studies ( 26 ). NO increasing results in a cascade reaction and then free radicals' production.…”
Background and purpose:
Mercuric chloride (Merc) can cause kidney toxicity. Harmine (Harm), an herbal alkaloid has various pharmacological and medicinal effects mainly because of its antioxidant activity. In this study, therefore, Harm's protective mechanisms on Merc-induced nephrotoxicity in BALB/c male mice were investigated.
Experimental approach:
Forty-eight male mice were randomly divided into six groups (n = 8). Groups were received saline, Merc (0.5 mL/day of 0.5 ppm aqueous), Harm (5, 10, 15 mg/kg/day), Merc + Harm (5, 10, 15 mg/kg/day) for 14 consecutive days. Saline and Harm were administrated intraperitoneally and Merc dissolved in drinking water. Urea and creatinine serum levels, body weight, kidney weight, quantitative and qualitative histological alterations, apoptosis rate, total antioxidant capacity (TAC), superoxide dismutase (SOD), and nitric oxide (NO) levels were evaluated.
Findings/Results:
There was a significant reduction in total body and kidney weights, renal histological criteria, TAC, SOD levels in the Merc group compared to the control group (
P
< 0.05), whereas these parameters in the Merc + Harm groups, were significantly increased compared to the Merc group (
P
< 0.05). Urea and creatinine serum levels, levels of NO, and apoptosis were significantly higher in the Merc group than the control, while these parameters were decreased in the Merc + Harms groups in comparison with the Merc group (
P
< 0.05).
Conclusion and implications:
Harm protected Merc-induced renal damage in mice. This protection was observed in both histological and biochemical respects. The beneficial effect of Harm was related to its antioxidant properties that diminish NO production and apoptosis induction in the kidney.
“…At the end of the equilibration period, dose-response curves for norepinephrine (NA, 10 −9 , 3 × 10 −9 , 10 −8 , 3 × 10 −8 , 10 −7 , 3 × 10 −7 , 10 −6 , 3 × 10 −6 , and 10 −5 mol/L) in the presence and absence of endothelium were obtained in aortic rings in a cumulative manner. To analyse the participation of NO on the response of NA, the NO synthase inhibitor L-NAME (L-NG-Nitroarginine methyl ester, 10 −4 mol/L) [ 24 ] was added 30 min before the concentration-response curves were performed.…”
We investigated the protective effects and mechanism of glutathione (GSH) on vascular hyporesponsiveness induced by bile duct ligation (BDL) in a rat model. Seventy-two male Sprague-Dawley rats were randomly divided into four groups: a NS group, a GSH group, a BDL + NS group, and a BDL + GSH group. GSH was administrated into rats in the GSH and BDL + GSH groups by gastric gavage. An equal volume of normal saline was, respectively, given in the NS group and BDL + NS group. Blood was gathered for serological determination and thoracic aorta rings were isolated for measurement of isometric tension. Obstructive jaundice led to a significant increase in the serum total bilirubin, AST, and ALT levels. The proinflammatory cytokines levels (TNF-α and IL-1β), concentration of NO, and oxidative stress markers (MDA and 3-NT) were increased as well. All of those were reduced by the treatment of GSH. Meanwhile, contraction of aorta rings to NA and vasorelaxation to ACh or SNP in the BDL group rats were markedly decreased, while GSH administration reversed this change. Our findings suggested that GSH supplementation attenuated overexpressed ONOO(−) from the reaction of excessive NO with O2
∙- and protected against obstructive jaundice-induced vascular hyporesponsiveness in rats.
“…This effect was mediated by increased production of NO because of the stimulation of eNOS. It is interesting to note that this increase occurred even when there was oxidative stress, suggesting a state of inclination toward NO 90 (Figure 2). Figure 2. Effect of low/high mercury exposure on endothelium-derived vasoactive factors.…”
Section: Mercury Exposure Oxidative Stress and No Signalingmentioning
Vascular endothelium plays a vital role in the organization and function of the blood vessel and maintains homeostasis of the circulatory system and normal arterial function. Functional disruption of the endothelium is recognized as the beginning event that triggers the development of consequent cardiovascular disease (CVD) including atherosclerosis and coronary heart disease. There is a growing data associating mercury exposure with endothelial dysfunction and higher risk of CVD. This review explores and evaluates the impact of mercury exposure on CVD and endothelial function, highlighting the interplay of nitric oxide and oxidative stress.
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