The Possible Ameliorative Effect of Curcumin on Atrazine-Induced Oxidative Stress, DNA Damage, Mitochondrial Dysfunction, and Apoptosis in the Kidney of Adult Male Albino Rats

Objective: Exposure to ultraviolet B (UVB) can cause skin damage through oxidative stress, DNA damage, and apoptosis. Keratinocyte growth factor (KGF) has been shown to reduce the content of intracellular reactive oxygen species (ROS) following UVB exposure, a role that is crucial for the efficient photoprotection of skin. The present study evaluated the photoprotective effect of KGF-2 on UVB-induced skin damage and explored its potential molecular mechanism.Methods: To evaluate the effect of KGF-2 on UVB-induced damage ex vivo, a human epidermal full-thickness skin equivalent was pretreated without or with KGF-2 and then exposed to UVB and the levels of histopathological changes, DNA damage, inflammation, and apoptosis were then evaluated. The ability of KGF-2 to protect the cells against UVB-inflicted damage and its effect on ROS production, apoptosis, and mitochondrial dysfunction were determined in HaCaT cells.Results: Pretreatment of the epidermis with KGF-2 ameliorated the extent of photodamage. At the cellular level, KGF-2 could attenuate ROS production, apoptosis, DNA damage, and mitochondrial dysfunction caused by UVB exposure. KGF-2 could also activate the aryl hydrocarbon receptor (AhR) to trigger the Nrf2 signaling pathway.Conclusion: Taken together, our findings suggested that KGF-2 could ameliorate UVB-induced skin damage through inhibiting apoptosis, reducing oxidative stress, and preventing DNA damage and mitochondrial dysfunction via regulating AhR/Nrf2 signaling pathway.

Download Full-text

Ameliorative Effect of Vitamin C against Monosodium Glutamate Induced Toxicity on Testes and Cauda Epididymal Sperm Reserves in Adult Male Albino Rats

Ain Shams Journal of Forensic Medicine and Clinical Toxicology ◽

10.21608/ajfm.2013.19409 ◽

2013 ◽

Vol 20 (1) ◽

pp. 199-220

Author(s):

Enas El-Maddah ◽

Mona Abo El-Noor ◽

Mona Abd El-Azeem

Keyword(s):

Vitamin C ◽

Adult Male ◽

Monosodium Glutamate ◽

Albino Rats ◽

Epididymal Sperm ◽

Ameliorative Effect

Download Full-text

Ameliorating Iron Overload in Intestinal Tissue of Adult Male Rats: Quercetin vs Deferoxamine

Journal of Toxicology ◽

10.1155/2018/8023840 ◽

2018 ◽

Vol 2018 ◽

pp. 1-13 ◽

Cited By ~ 1

Author(s):

Arwa A. El-Sheikh ◽

Shimaa Hamed Ameen ◽

Samaa Salah AbdEl-Fatah

Keyword(s):

Oxidative Stress ◽

Iron Overload ◽

Adult Male ◽

Caspase 3 ◽

Iron Chelation ◽

Male Rats ◽

Albino Rats ◽

Tissue Iron ◽

Small Intestinal

Objective. The aim of our study is to compare the role of the new natural alternative (Quercetin) with the current iron-chelation therapy (Deferoxamine (DFO)) in the effect of iron overload on small intestinal tissues and to investigate the possible underlying molecular mechanisms of such toxicity. Methods. Forty-two adult male albino rats were divided into six groups: control groups, DFO, Quercetin, iron overload, iron overload+DFO, and iron overload+Quercetin groups. Animals received daily intraperitoneal injection of Deferoxamine (125 mg /kg), Quercetin (10 mg/kg), and ferric dextran (200 mg/kg) for 2 weeks. Results. Iron overloaded group showed significant increase in serum iron, total iron binding capacity (TIBC), transferrin saturation percentage (TS %) hepcidin (HEPC), serum ferritin, nontransferrin bound iron (NTBI), and small intestinal tissues iron levels. Iron overload significantly increased the serum oxidative stress indicator (MDA) and reduced serum total antioxidant capacity (TAC). On the other hand, iron overload increased IL6 and reduced IL10 in small intestinal tissues reflecting inflammatory condition and increased caspase 3 reactivity indicating apoptosis and increased iNOs expressing cell indicting oxidative stress especially in ileum. In addition, it induced small intestinal tissues pathological alterations. The treatment with Quercetin showed nonsignificant differences as compared to treatment with DFO that chelated the serum and tissue iron and improved the oxidative stress and reduced tissue IL6 and increased IL10 and decreased caspase 3 and iNOs expressing cells in small intestinal tissues. Moreover, it ameliorated the iron overload induced pathological alterations. Conclusion. Our study showed the potential role of Quercetin as iron chelator like DFO in case of iron overload induced small intestinal toxicity in adult rats because of its serum and tissue iron chelation, improvement of serum, and small intestinal oxidative stress, ameliorating iron induced intestinal inflammation, apoptosis, and histopathological alterations.

Download Full-text

Phorate triggers oxidative stress and mitochondrial dysfunction to enhance micronuclei generation and DNA damage in human lymphocytes

Saudi Journal of Biological Sciences ◽

10.1016/j.sjbs.2019.04.008 ◽

2019 ◽

Vol 26 (7) ◽

pp. 1411-1417 ◽

Cited By ~ 2

Author(s):

Quaiser Saquib ◽

Mohammad Faisal ◽

Sabiha Mahmood Ansari ◽

Rizwan Wahab

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Mitochondrial Dysfunction ◽

Human Lymphocytes

Download Full-text

Chronic Addiction to Tramadol and Withdrawal Effect on the Spermatogenesis and Testicular Tissues in Adult Male Albino Rats

Pharmacology ◽

10.1159/000496424 ◽

2019 ◽

Vol 103 (3-4) ◽

pp. 202-211 ◽

Cited By ~ 3

Author(s):

Marwan Abdel-Latif Ibrahim ◽

Alaa-Eldin Salah-Eldin

Keyword(s):

Oxidative Stress ◽

Antioxidant Enzymes ◽

Adult Male ◽

Rna Extraction ◽

B Cell Lymphoma ◽

Experimental Period ◽

Male Rats ◽

Control Group ◽

Albino Rats ◽

Withdrawal Effect

Aim: The present study aimed to elucidate the effects of tramadol on the testicular functions of adult male rats due to the chronic usage of tramadol and the effect of its withdrawal. Method: Adult male albino rats were classified into the following 3 groups: (I) a control administered with normal saline and (II) tramadol-treated rats (40 mg/kg b.w. orally) for 21 successive days; and (III) like the rats in the second group but kept for 4 weeks after the last tramadol dose to study the effect of tramadol withdrawal. At the end of the experimental period, blood was collected and specimens from testis were taken for histopathological, biochemical, and molecular studies. A reverse transcription-polymerized chain reaction after RNA extraction from specimens was detected for the anti-apoptotic and pro-apoptotic genes in testicular tissues. Also, malondialdehyde (MDA) was measured in tissues homogenate and antioxidant enzymes activities were evaluated. Results: The results of this study demonstrated histological changes in testicular tissues in groups II and III compared to the control group, accompanied with increased apoptotic index and proved by increased B-cell lymphoma-2 (Bcl-2) associated-X-protein and caspase-3 expression, whereas anti-apoptotic Bcl-2 markedly decreased. Moreover, in tramadol-abused and -withdrawal groups, the MDA level increased, while the antioxidant enzymes activity decreased and revealed oxidative stress, indicating that tramadol is harmful at the cellular level and can induce apoptotic changes in testicular tissues. The withdrawal effect showed signs of improvement, but it did not return to normal levels. Conclusions: It could be concluded that the administration of tramadol causes abnormalities on testicular tissues associated with oxidative stress, which confirmed the risk of increased oxidative stress on testicular tissues due to tramadol abuse.

Download Full-text