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All Journal African Journal of Biochemistry and Molecular Biology Research Open Access DRIVERset
Ibor, Mbang Edet
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Biochemistry, Genetics & Molecular Biology

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Bifenthrin Causes Kidney Damage via Induction of Oxidative Stress, Activation of Pro-Inflammatory Cytokines, and Up-Regulation of Apoptosis in Wistar Rats Ujong, Ujong Peter; Ibor, Mbang Edet
African Journal of Biochemistry and Molecular Biology Research Vol 1 No 1 (2024): African Journal of Biochemistry and Molecular Biology Research
Publisher : Darul Yasin Al Sys

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.58578/ajbmbr.v1i1.3654

Abstract

This study investigated the role of oxidative stress, inflammation, and apoptosis in bifenthrin-induced kidney damage in Wistar rat models. Adult male rats (110-300g) were divided into three groups of 10 rats each. Group 1 served as the normal control, while groups 2-3 were orally given 1 mg/ kg body weight bifenthrin for 14 and 28 days respectively. The results revealed that bifenthrin administration caused a significant (p<0.05) decrease in renal antioxidant enzymes such as superoxide dismutase, catalase, glutathione, glutathione S-transferase, and glutathione peroxidase. Conversely, malondialdehyde levels were significantly (p<0.05) increased. Pro-inflammatory cytokines TNF-α, IL1-β, IL-6, COX-2, iNOS, LTE B4, and PGE2 were significantly (p<0.05) elevated, highlighting an inflammatory response. Additionally, the apoptotic markers, caspase-3, and BAX were significantly (p<0.05) increased, while BCL-2, an anti-apoptotic protein, was significantly (p<0.05) decreased, indicating enhanced apoptosis. Renal function markers, creatinine, and urea were also significantly (p<0.05) elevated in bifenthrin-induced groups. Furthermore, the histopathology results revealed morphological damages in the kidneys of groups 2 and 3 animals These findings demonstrate bifenthrin's potential to cause significant oxidative stress, inflammation, apoptosis, and structural damage in renal tissues.
Bifenthrin Causes Kidney Damage via Induction of Oxidative Stress, Activation of Pro-Inflammatory Cytokines, and Up-Regulation of Apoptosis in Wistar Rats Ujong, Ujong Peter; Ibor, Mbang Edet
African Journal of Biochemistry and Molecular Biology Research Vol 1 No 1 (2024): African Journal of Biochemistry and Molecular Biology Research
Publisher : Darul Yasin Al Sys

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.58578/ajbmbr.v1i1.3654

Abstract

This study investigated the role of oxidative stress, inflammation, and apoptosis in bifenthrin-induced kidney damage in Wistar rat models. Adult male rats (110-300g) were divided into three groups of 10 rats each. Group 1 served as the normal control, while groups 2-3 were orally given 1 mg/ kg body weight bifenthrin for 14 and 28 days respectively. The results revealed that bifenthrin administration caused a significant (p<0.05) decrease in renal antioxidant enzymes such as superoxide dismutase, catalase, glutathione, glutathione S-transferase, and glutathione peroxidase. Conversely, malondialdehyde levels were significantly (p<0.05) increased. Pro-inflammatory cytokines TNF-α, IL1-β, IL-6, COX-2, iNOS, LTE B4, and PGE2 were significantly (p<0.05) elevated, highlighting an inflammatory response. Additionally, the apoptotic markers, caspase-3, and BAX were significantly (p<0.05) increased, while BCL-2, an anti-apoptotic protein, was significantly (p<0.05) decreased, indicating enhanced apoptosis. Renal function markers, creatinine, and urea were also significantly (p<0.05) elevated in bifenthrin-induced groups. Furthermore, the histopathology results revealed morphological damages in the kidneys of groups 2 and 3 animals These findings demonstrate bifenthrin's potential to cause significant oxidative stress, inflammation, apoptosis, and structural damage in renal tissues.
Co-Authors Ujong, Ujong Peter