Atrazine (ATR) is an extensively used herbicide that is often found in drinking water and waterways. After metabolization and excretion in the liver, ATR residues or its metabolites were found in tissues causing harmful effects mainly to the endocrine system and liver. This study aimed to elucidate the toxic impact of ATR on the liver and possible ameliorative effects of L-carnitine (LC). It utilized 30 adult male albino rats divided into three equal groups; the control group received 0.5 cc distilled water orally for 14 days, an ATR-treated group received ATR in a dose of 400 mg/kg BW dissolved in distilled water by oral gavage daily for 14 days, and a protected group (ATR + LC) received 400 mg/kg BW of ATR dissolved in distilled water, plus 100 mg/kg LC dissolved in distilled water by oral gavage daily for 14 days. At the end of the experiment, the liver tissue was prepared for histological and biochemical analyses and showed significant elevation of liver enzymes and oxidative parameters, altered expression of apoptotic and antiapoptotic genes, and hepatic degenerative changes in the ATR-treated group. In conclusion, atrazine induces oxidative stress, inflammation, and apoptosis in the liver of rats, and these toxic effects can be alleviated by L-carnitine.
Cyclooxygenase-2 (COX-2), an inducible isoform of cyclooxygenase, has been reported to be correlated with tumorigenesis, tumor progression, and metastasis. We aimed to evaluate the association between COX-2 (rs2745557) polymorphism and prostate cancer (PCa), benign prostate hyperplasia (BPH) risk. We also assessed the influence of other risk factors such as obesity, smoking, diabetes in modulating the risk of PCa in Egyptian men. COX-2 (rs2745557) was genotyped in 112 PC patients, 111 BPH and 120 subjects as a control group. COX-2 and PSA levels were measured by ELISA. We found that GG genotype was associated with a 17-fold increased risk for PCa and 20-fold increased the risk for BPH more than AA genotype. Also, G allele carriers of COX-2 were associated with metastatic cancer (OR = 1.3, P < 0.05) and disease aggressiveness (OR = 3.5, P < 0.001). The coexistence of obesity, smoking, or diabetes with GG genotype may lead to increasing the risk of developing BPH (OR = 3.3, 4, and 2.7, respectively) and of developing PCa (OR = 2.9, 4.9, and 3.2, respectively). Our results showed evidence suggesting the involvement of the COX-2 (rs2745557) polymorphism and its protein in PCa or BPH initiation and progression. Also, the coexistence of COX-2 (rs2745557) and obesity, smoking, or diabetes may lead to the development of PCa or BPH.
Myocardial injury influenced by cisplatin (Cis) is a compelling reason to hunt out a treatment modality to overcome such a threat in cisplatin-treated patients. Breast Milk mesenchymal stem cells (Br-MSCs) are a non-invasive, highly reproducible source of stem cells. Herein, we investigate Br-MSCs' role in cardiotoxicity induced by cisplatin. Rats were divided into; control, Cis-treated (received 12 mg/kg single intraperitoneal injection), BrMSCs-treated (received single intraperitoneal injection of 0.5 ml sterilized phosphate-buffered saline containing 2 × 107 cells of Br-MSCs); metformin-treated (received 250 mg/kg/day orally) and BrMSCs + metformin + Cis treated groups. At the experiment end, serum creatine kinase (CK-MB) and cardiac troponin T (cTnT) activates were estimated, cardiac malondialdehyde (MDA), superoxide dismutase (SOD), interleukin-1ß (IL-1ß), tumor necrosis factor-α (TNF-α) levels were measured, cardiac expression of Bax and Bcl-2 and AMP-activated protein kinase (AMPK), as well as heart histopathology, were evaluated. Study results showed that Cis explored acute cardiotoxicity evidenced by deteriorated cardiac indices, induction of oxidative stress, and inflammation with myocardium histological alterations. Treatment with Br-MSCs restored heart function and structure deteriorated by Cis injection. The antioxidant/anti-inflammatory/anti-apoptotic results of Br-MSCs were supported by AMPK activation denoting their protective role against cisplatin-induced cardiac injury. These results were superior when metformin was added to the treatment protocol.
Introduction/objective Ovarian cancer is the 6th leading cause of mortality in women, killing more women than any other reproductive system cancer. We studied the expression of serum micro-ribonucleic acid-21 (miRNA-21) in ovarian cancer patients and explored associations with diagnosis, clinicopathological parameters, and prognosis. Methods Real-time fluorescence-quantitative polymerase chain reaction was used to examine the relative expression of miRNA-21 in serum. Cancer antigen 125 (CA-125) levels were measured using an enzyme immunoassay test kit (ELISA). Results Serum miR-21 expression was significantly elevated in ovarian cancer patients compared to controls (p < 0.001). The same was true for CA-125 serum levels, which were also significantly in cancer patients (p < 0.001). The sensitivity and specificity of miR-21 detection in the diagnosis of ovarian cancer were 96%, 88% versus 74%, and 80% for CA-125. Conclusions miR-21 is highly expressed in the serum of ovarian cancer patients and may be important in the development and progression of ovarian cancer, with more sensitivity and specificity than CA-125. Our results suggest that circulating serum miRNA-21 is a promising tumor marker for use in the diagnosis and prognosis of ovarian cancer.
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