The effect of thymoquinone treatment on the combined renal and pulmonary toxicity of cisplatin and diesel exhaust particles

Ali, Badreldin H.; Za’abi, Mohammed Al; Shalaby, Asem; Manoj, P; Waly, Mostafa I.; Yasin, Javed; Fahim, Mohamed A.

doi:10.1177/1535370215579013

Cited by 27 publications

(19 citation statements)

References 42 publications

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“…Treatment with GA did not show significant ameliorative effect on the observed changes. In line with these findings, recent studies by Ali et al (2015) and Nemmar et al (2015) showed that repeated exposure to DP potentiated cisplatin-induced nephrotoxicity. Systolic blood pressure was increased, levels of nitric oxide were elevated and the renal tubular necrosis was aggravated.…”

Section: Discussionsupporting

confidence: 72%

“…Recently, it has been suggested that there is a link between exposure to air pollution and cardiovascular disease in kidney transplant recipients (Spencer‐Hwang et al, ). Moreover, in vivo experimental studies have provided evidence that exposure to DP in the lung aggravates the renal, pulmonary, and systemic effects of cisplatin‐induced acute renal failure in rats (Nemmar et al, ; Nemmar et al, ; Ali et al, ).…”

Section: Introductionmentioning

confidence: 99%

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Effect of diesel exhaust particles on renal vascular responses in rats with chronic kidney disease

Suleimani

Mahruqi

Za’abi

et al. 2016

Environmental Toxicology

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Several recent studies have indicated the possible association between exposure to particulate air pollution and the increased rate of morbidity and mortality in patients with kidney diseases. The link of this observation to vascular damage has not been adequately addressed. Therefore, this study aims to investigate possible vascular damage that might be associated with exposure to diesel exhaust particles (DP) in adenine (AD)-induced chronic kidney disease (CKD) in rats, and the possible ameliorative effect of gum acacia (GA). CKD was induced by feeding AD (0.75%, w/w), and DP (0.5 mg/kg) was instilled intratracheally every second day and GA was given concomitantly in the drinking water at a dose of 15% w/v. All treatments were given concomitantly for 28 days. Changes in renal blood flow (RBF) and systolic and diastolic blood pressure were monitored in these animals after anesthesia, together with several other endpoints. Exposure to DP significantly reduced RBF and this was significantly potentiated in AD-treated rats. Phenylephrine-induced decreases in RBF and increases in systolic and diastolic blood pressure were severely potentiated in rats exposed to DP, and these actions were significantly augmented in AD-treated rats. GA did not significantly affect the vascular impairment induced by AD and DP given together. This study provides experimental evidence that exposure to particulate air pollution can exacerbate the vascular damage seen in patients with CKD. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 541-549, 2017.

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Section: Discussionsupporting

confidence: 72%

Section: Introductionmentioning

confidence: 99%

Effect of diesel exhaust particles on renal vascular responses in rats with chronic kidney disease

Suleimani

Mahruqi

Za’abi

et al. 2016

Environmental Toxicology

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“…Ali et al [61] studied the interaction between cisplatin (CP) nephrotoxicity and a single exposure to diesel exhaust particles and the concurrent treatment with TQ (20 mg/kg, orally) in rats. The results showed that several biochemical, physiological, and histopathological alterations contained decreased growth and Cr clearance and increased IL-6, plasma neutrophil gelatinase-associated lipocalin, C-reactive protein, urea and Cr concentrations, and urinary N-acetyl-b-D-glucosaminidase (NAG) activities induced by CP, and were significantly abrogated by TQ.…”

Section: Resultsmentioning

confidence: 99%

“…The results showed that several biochemical, physiological, and histopathological alterations contained decreased growth and Cr clearance and increased IL-6, plasma neutrophil gelatinase-associated lipocalin, C-reactive protein, urea and Cr concentrations, and urinary N-acetyl-b-D-glucosaminidase (NAG) activities induced by CP, and were significantly abrogated by TQ. Also, TQ significantly resolved potentiated indices of oxidative injuries in the kidney tissues, and induced renal tubular necrosis induced by CP and diesel exhaust particles [61]. …”

Section: Resultsmentioning

confidence: 99%

An Overview on Renoprotective Effects of Thymoquinone

et al. 2018

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Background: Kidneys as vital organs remove waste material from blood. Additionally, they may also have a role in the electrolyte balance, regulation of blood pressure, and red blood cell genesis. Kidney diseases may be caused by several factors such as ischemia/reperfusion injury, diabetes, and nephrotoxic agents. Oxidative stress and inflammation are involved in the pathogenesis and progression of kidney diseases. Traditionally, natural antioxidants are used for treatment of renal failure in various countries. Summary: People usually select natural antioxidants since they have an opinion that herbal medicine has not any important side effects. Nigella sativa is a flavoring herb that is widely used as a condiment and as a remedy for many disorders. Thymoquinone (TQ), the most important component of black seeds, mainly oil, is considered as an active agent responsible for a lot of the seed’s useful effects. This review describes the protective roles and related mechanisms of TQ against renal disorders. The search terms, including TQ, antioxidant, renal ischemia-reperfusion, diabetic nephropathy, and nephrotoxic agent were searched in scientific databases. TQ showed anti-inflammatory and antioxidant properties in animal and in vitro models of several renal diseases caused by inflammation and oxidative stress. Key Messages: Experimental studies have shown beneficial effects of TQ against renal diseases; however, well-designed clinical trials in humans are required to confirm these effects.

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“…Interestingly, Budinger et al (2011) suggested that IL-6 is significantly associated with PM-induced thrombogenic effects independent of other inflammatory markers [ 61 ]. Two studies have been published examining the effect of anti-inflammatory agents on thrombogenic factors in mice following exposure to DEP (15–30 μg) [ 66 , 67 ]. Both studies demonstrated a critical role for inflammation in mediating DEP-induced thrombotic effects [ 66 , 67 ].…”

Section: In Vivo Studies In Animalsmentioning

confidence: 99%

Ambient air pollution and thrombosis

2018

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Air pollution is a growing public health concern of global significance. Acute and chronic exposure is known to impair cardiovascular function, exacerbate disease and increase cardiovascular mortality. Several plausible biological mechanisms have been proposed for these associations, however, at present, the pathways are incomplete. A seminal review by the American Heart Association (2010) concluded that the thrombotic effects of particulate air pollution likely contributed to their effects on cardiovascular mortality and morbidity. The aim of the current review is to appraise the newly accumulated scientific evidence (2009–2016) on contribution of haemostasis and thrombosis towards cardiovascular disease induced by exposure to both particulate and gaseous pollutants.Seventy four publications were reviewed in-depth. The weight of evidence suggests that acute exposure to fine particulate matter (PM2.5) induces a shift in the haemostatic balance towards a pro-thrombotic/pro-coagulative state. Insufficient data was available to ascertain if a similar relationship exists for gaseous pollutants, and very few studies have addressed long-term exposure to ambient air pollution. Platelet activation, oxidative stress, interplay between interleukin-6 and tissue factor, all appear to be potentially important mechanisms in pollution-mediated thrombosis, together with an emerging role for circulating microvesicles and epigenetic changes.Overall, the recent literature supports, and arguably strengthens, the contention that air pollution contributes to cardiovascular morbidity by promoting haemostasis. The volume and diversity of the evidence highlights the complexity of the pathophysiologic mechanisms by which air pollution promotes thrombosis; multiple pathways are plausible and it is most likely they act in concert. Future research should address the role gaseous pollutants play in the cardiovascular effects of air pollution mixture and direct comparison of potentially susceptible groups to healthy individuals.

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The effect of thymoquinone treatment on the combined renal and pulmonary toxicity of cisplatin and diesel exhaust particles

Cited by 27 publications

References 42 publications

Effect of diesel exhaust particles on renal vascular responses in rats with chronic kidney disease

Effect of diesel exhaust particles on renal vascular responses in rats with chronic kidney disease

An Overview on Renoprotective Effects of Thymoquinone

Ambient air pollution and thrombosis

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