Effect of exposure to Benzene on oxidative stress and the functions of liver and kidney of male Albino Rat

El-Shakour, Alia Abd; El-Ebiarie, Ahmad S.; Ibrahim, Yasser; Moneim, Ahmed Abdel; El-Mekawy, Asmaa

doi:10.5455/jeos.20141223050552

Cited by 17 publications

(18 citation statements)

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“…This notion is consistent with previous studies which showed that exposure to GV is associated with the induction of OS [22,24,25]. MDA is an end product of lipid peroxidation, a pathogenic step in OS-induced tissue damage.…”

Section: Discussionsupporting

confidence: 93%

“…Furthermore, the kidney is a major organ for the excretion of metabolic waste, and a significant increase in the levels of serum Cr -, Ur, UA, and electrolytes may indicate impairment of the excretory and concentration functions of the kidney, which are responsible for maintenance of a constant extracellular environment by excreting and regulating water and electrolyte balance. This idea is supported by previous studies with similar findings [22,31].…”

Section: Discussionsupporting

confidence: 90%

“…It is also posited that service station workers are exposed to gasoline inhalation for many hours per week and approximately 8086 minutes per year. Interestingly, some gasoline compounds are nephrotoxic even at low concentrations [22]. The rising number of people exposed to gasoline compounds for various reasons, including industrial and domestic purposes, may explain the increasing nephrotoxicity.…”

Section: Introductionmentioning

confidence: 99%

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Tubular Necrosis, Acid-Base and Electrolyte Abnormalities Associated with Gasoline Vapour-induced Nephrotoxicity

2020

AJUN

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Introduction: This study aimed to assess the effect of exposure to gasoline vapor (GV) on the histomorphology and biochemical markers of renal function in rats. Methods: Twenty-four mature Wistar Albino rats weighing 180–200 g were randomly divided into two groups (n = 12 per group). Animals in group 1 (G1) served as unexposed controls, while animals in group 2 (G2) were exposed to GV for 35 days. At the end of the exposure, the animals were sacrificed, and blood samples were collected for biochemical analysis while the kidneys were removed and processed for histopathological evaluation. Results: Serum biochemical markers of renal function in the exposed group differed significantly (p< 0.05) from the unexposed group in urea (45.16 ± 1.00mg/dl versus(vs) 13.20 ± 0.69 mg/dl), creatinine (1.16 ± 0.27mg/dl vs 0.38 ± 0.10mg/dl), uric acid (3.66 ± 0.82mmol/L vs 1.96 ± 0.08mmol/L), potassium (6.90 ± 0.27mmol/L vs 3.57 ± 0.26mmol/L), sodium (182.60 ± 3.21mmol/L vs 141.33 ± 10.46mmol/L), chloride (119.00 ± 1.58mmol/L vs 103.33 ± 2.07mmol/L), pH (6.82 ± 0.22 vs 7.38 ± 0.25), bicarbonate (16.60 ± 5.03mmol/L vs 26.50 ± 3.45mmol/L), and glucose (125.60 ± 16.23mg/ dl vs 83.33 ± 4.46mg/dl). Histopathological examination of kidney sections revealed areas of degenerative and necrotic changes in the glomerulus, tubules, and renal vasculature, particularly in the cortical portion of the kidney. Conclusion: Chronic exposure to gasoline compounds may be associated with significant structural and biochemical derangements in kidney function.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

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Tubular Necrosis, Acid-Base and Electrolyte Abnormalities Associated with Gasoline Vapour-induced Nephrotoxicity

2020

AJUN

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“…Experimental studies have found that benzene can be enzymatically bioactivated to reactive intermediates (catechol, hydroquinone, phenol) which can produce reactive oxygen species (ROS) through redox cycling as illustrated in Fig. 1 [5] , [6] . On this basis, serum reactive oxygen metabolites have been recently suggested as biomarkers in oxidative stress assessment [7] , [8] .…”

Section: Introductionmentioning

confidence: 99%

8-Hydroxydeoxyguanosine as a biomarker of oxidative DNA damage in workers exposed to low-dose benzene

et al. 2017

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“…Many human and animal studies [103,[125][126][127][128][129][130] A -gasoline (parent nephrotoxicant) may bind to the membrane lipid bilayer and proteins due to its high lipophilicity, leading to damage to the membrane bilayer and proteins, which causes inhibition of Na + /K + /ATPase activity, which in turn leads to disruption of ion homeostasis and cell injury; B -alternatively, gasoline may undergo biotransformation to reactive intermediates (e.g., 1,2,3-benzenetriol and benzequinone) that bind covalently to macromolecules and in turn alter their activity (e.g., inhibition of Na + /K + /ATPase), resulting in cell injury; C -additionally, gasoline may increase in the renal cells directly after being biotransformed into reactive intermediates through redox cycling. The resultant increase in ROS may cause oxidative damage and cell injury; D -finally, the generated ROS may cause disruption of the immune system, leading to immune perturbation, and a resultant induction of autoimmunity.…”

Section: Hepatotoxicitymentioning

confidence: 99%

Recent advances in occupational and environmental health hazards of workers exposed to gasoline compounds

Ekpenyong

Asuquo

2017

Int J Occup Med Environ Health

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The impact of health and environmental hazards, associated with the constituents of gasoline, on occupationally exposed workers has been recorded over the past few decades. However, the scientific literature on their pathogenic potential remains incomplete, which could affect the current understanding of the associated health risks. This review provides current information based on recently improved research techniques to evaluate gasoline toxicity profiles for humans. Our current knowledge provides insight into the intricate mechanism of gasoline-induced adverse effects, including the formation of reactive metabolites via bio-activation and subsequent generation of reactive oxygen species (ROS) and oxidative stress, which are involved in multiple mechanisms that are central to the aetiology of gasoline-induced toxicity. These mechanisms include covalent binding to deoxyribonucleic acid (DNA), leading to oxidative damage, tumor-suppression gene activity, and activation of pro-oncogenes. Furthermore, it results in induction of autoimmunity and local inflammatory responses, disruption of multiple neurotransmitters and immune cell function, derangement of various enzyme activities (e.g., sodiumpotassium adenosine triphosphate (Na + /K + /ATPase) activity, cytochrome P450 (CYP450), nitric oxide synthase (NOS), antioxidant enzyme activities, etc.), conjugation of bile, and non-specific cell membrane interaction, leading to damage of the membrane lipid bilayer and proteins. Available data suggests that exposure to gasoline or gasoline constituents have the potential to cause different types of illnesses. The data highlights the need to maintain safety measures via suitable research, medical surveillance, regulatory control, life style modification, early detection, and intervention to minimize exposure and manage suspected cases. They also present novel opportunities to design and develop effective therapeutic strategies against gasoline-induced detrimental effects. Int J Occup Med Environ Health 2017;30(1):1-26

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Effect of exposure to Benzene on oxidative stress and the functions of liver and kidney of male Albino Rat

Cited by 17 publications

References 0 publications

Tubular Necrosis, Acid-Base and Electrolyte Abnormalities Associated with Gasoline Vapour-induced Nephrotoxicity

Tubular Necrosis, Acid-Base and Electrolyte Abnormalities Associated with Gasoline Vapour-induced Nephrotoxicity

8-Hydroxydeoxyguanosine as a biomarker of oxidative DNA damage in workers exposed to low-dose benzene

Recent advances in occupational and environmental health hazards of workers exposed to gasoline compounds

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