Lack of reversal of oxidative damage in renal tissues of lead acetate‐treated rats

Oyagbemi, Ademola Adetokunbo; Omobowale, Temidayo Olutayo; Akinrinde, Akinleye Stephen; Saba, Adebowale Benard; Ogunpolu, Blessing Seun; Daramola, Oluwabusola

doi:10.1002/tox.21994

Cited by 110 publications

(57 citation statements)

References 40 publications

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“…The catalase (CAT) activity was determined according to the method of Sinha [14]. Superoxide dismutase (SOD) was determined by measuring the inhibition of auto-oxidation of epinephrine at pH 10.2 as described by Misra and Fridovich [15] with slight modification as described by Oyagbemi et al [16]. The MDA level measured as described by Varshney and Kale [17].…”

Section: Biochemical Assaysmentioning

confidence: 99%

Sodium arsenite-induced cardiovascular and renal dysfunction in rat via oxidative stress and protein kinase B (Akt/PKB) signaling pathway

et al. 2017

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(2017) Sodium arsenite-induced cardiovascular and renal dysfunction in rat via oxidative stress and protein kinase B (Akt/PKB) signaling pathway, Redox Report, 22:6, 467-477, DOI: 10.1080/13510002.2017 Objectives: Arsenic is a ubiquitous element that is widely distributed in the environment to which man and animals are exposed. Cardiovascular disease is one of the aftermaths of chronic arsenic exposure-related morbidity and mortality. This study sought to investigate the possibility of reversal from arsenic-induced cardio-renal toxicity following exposure and subsequent withdrawal. The study also seeks to understand the mechanism of action of this reversal. Methods: Rats were orally exposed to sodium arsenite at 10, 20 and 40 mg/kg daily for 4 weeks followed by 4 weeks of withdrawal. Results: Exposure to arsenic caused a significant increase in malondialdehyde, H 2 O 2 generation but decrease total thiol and reduced glutathione levels in both cardiac and renal tissues. Furthermore, increases in superoxide dismutase, glutathione-S-transferase and catalase with significant increases in glutathione peroxidase activities were observed in the cardiac tissues. On the contrary, a significant reduction in the renal antioxidant enzyme activity was recorded following exposure. Also, antioxidant defense system did not return to apparent values after arsenic withdrawal. Immunohistochemistry revealed a reduction in the expression of the prosurvival protein-protein kinase B (Akt/PKB) following exposure to arsenic and this was not reversed by withdrawal Discussion: Exposure to arsenic caused cardio-renal toxicity via induction of oxidative stress and down-regulation of Akt/PKB expressions.

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Section: Biochemical Assaysmentioning

confidence: 99%

Sodium arsenite-induced cardiovascular and renal dysfunction in rat via oxidative stress and protein kinase B (Akt/PKB) signaling pathway

et al. 2017

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“…Superoxide dismutase (SOD) was determined by the method of Misra and Fridovich (1972) with modification from our laboratory (Oyagbemi et al 2015), giving credence to the validation of the method. Briefly, 100 mg of epinephrine was dissolved in 100 mL distilled water and acidified with 0.5 mL concentrated hydrochloric acid.…”

Section: Determination Of Intestinal Superoxide Dismutase Activitymentioning

confidence: 99%

Antidiabetic and anti-oxidant activities of the methanol leaf extract of <i>Vernonia amygdalina</i> in alloxan-induced diabetes in Wistar rats

Adeoye

Oyagbemi

Adedapo

et al. 2017

JOMPED

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The methanolic leaf extract of Vernonia amygdalina (MLVA) was assessed to evaluate its antidiabetic potential in rats. Diabetes was induced in male Wistar rats by the administration of alloxan monohydrate at 100 mg/kg of body weight. After 48 h, rats with fasting blood glucose levels of 200 mg/dL and above were considered diabetic and used for the study. The experimental animals were grouped into five groups (A–E) of 10 animals each. Group A rats were non-diabetic normal control, Group B consisted of diabetic control rats that received no treatment, groups C, D and E rats were diabetic rats but treated with glibenclamide, 200 and 400 mg/kg doses of MLVA respectively. Blood samples were collected at days 14 and 28 after induction for haematological and serum biochemical indices such as triglycerides, LDL, cholesterols etc. The intestine was collected and intestinal homogenate was prepared for the antioxidant studies. The extract at 200 mg/kg and 400 mg/kg doses significantly (p < 0.05) reduced blood glucose levels in extract-treated diabetic rats and also significantly increased weight gain in these rats. Most haematological parameters in treated rats experienced, while platelets and neutrophils were decreased. Biochemical indices measured were reduced in MLVA-treated groups compared with diabetic control. Treatment with MLVA also produced significant (p < 0.05) decrease in markers of oxidative stress but increased levels of enzymic and non-enzymic antioxidant markers in intestinal homogenates of treated groups compared with diabetic control. This study showed that V. amygdalina has antihyperglycaemic and in vivo antioxidant effects.

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“…Environmental lead exposure cause significant pathological lesions on the renal systems of men and animals [18].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Performance of Date Palm Pollen on Urea and Creatinine Levels in Adult Female Rats Exposed to Lead Acetate Intoxication

Salim

2015

Int J of Biomed & Adv Res

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Background and objective: Exposure to lead continues to a serious public problem. The objective is to elucidate the effect of lead acetate exposure on serum Concentration of urea and creatinine in adult female rats. Methods:Forty-eight adults female rats divided in to four groups (12 rats/group) .Group 1, (T1), given date palm pollen (150 mg/kg. B.W.) Group 2,(T2) given lead acetate (10mg/kg. B.W.), group 3, (T3) given lead acetate (10mg/kg. B.W.) and date palm pollen (150 mg/kg. B.W) for 6 weeks, Group 4(Control), given distilled water. Serum concentration of urea and creatinine was evaluated via ELISA method for all groups. Results:The mean concentration of urea showed no significant difference between, (T1) and (T3) while in T2 a significant (p < 0.05) increase in urea concentration compared to T1&T3.There was no significant difference within groups in urea concentration. Group (T1) exposed to DPP showed no significant decrease in serum creatinine on zero, 14, 28 day & 42 day post exposure respectively. Group (T2) exposed to lead acetate showed significant increase of creatinine concentration compared with control and (T1) group.Group (T3) showed significant decrease in creatinine levels compared with T2 group and these levels become closely to control group. Histological changes indicated that DPP significantly meliorate the toxic effects of lead acetate in glomeruli, collecting tubules associated with obvious decrease in inflammatory response. Conclusion: DPP has the ability to counteract the toxic effect of lead acetate associated with improvement of renal histology and serum concentration of urea and creatinine.

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Lack of reversal of oxidative damage in renal tissues of lead acetate‐treated rats

Cited by 110 publications

References 40 publications

Sodium arsenite-induced cardiovascular and renal dysfunction in rat via oxidative stress and protein kinase B (Akt/PKB) signaling pathway

Sodium arsenite-induced cardiovascular and renal dysfunction in rat via oxidative stress and protein kinase B (Akt/PKB) signaling pathway

Antidiabetic and anti-oxidant activities of the methanol leaf extract of <i>Vernonia amygdalina</i> in alloxan-induced diabetes in Wistar rats

Evaluation of Performance of Date Palm Pollen on Urea and Creatinine Levels in Adult Female Rats Exposed to Lead Acetate Intoxication

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