Cobalt chloride toxicity elicited hypertension and cardiac complication via induction of oxidative stress and upregulation of COX-2/Bax signaling pathway

Abstract

<jats:p> Cobalt is a ferromagnetic metal with extensive industrial and biological applications. To assess the toxic effects of, and mechanisms involved in cobalt chloride (CoCl<jats:sub>2</jats:sub>)-induced cardio-renal dysfunctions. Male Wistar rats were exposed orally, daily through drinking water to 0 ppm (control), 150 ppm, 300 ppm, and 600 ppm of CoCl<jats:sub>2</jats:sub>, respectively. Following exposure, results revealed significant ( p &lt; 0.05) rise in markers of oxidative stress, but decreased activities of catalase, glutathione peroxidase, glutathione-S-transferase, and reduced glutathione content in cardiac and renal tissues. There were significant increases in systolic, diastolic, and mean arterial blood pressure at the 300- and 600-ppm level of CoCl<jats:sub>2</jats:sub>-exposed rats relative to the control. Prolongation of QT and QTc intervals was observed in CoCl<jats:sub>2</jats:sub> alone treated rats. Also, there were significant increases in the heart rates, and reduction in P wave, and PR duration of rats administered CoCl<jats:sub>2</jats:sub>. Histopathology of the kidney revealed peritubular and periglomerular inflammation, focal glomerular necrosis following CoCl<jats:sub>2</jats:sub> exposure. Further, cyclooxygenase-2 and B-cell associated protein X expressions were upregulated in the cardiac and renal tissues of CoCl<jats:sub>2</jats:sub>-exposed rats relative to the control. Combining all, results from this study implicated oxidative stress, inflammation, and apoptosis as pathologic mechanisms in CoCl<jats:sub>2</jats:sub>-induced hypertension and cardiovascular complications of rats. </jats:p>

Ethanolic Extract of Moringa oleifera Leaves Influences NF-κB Signaling Pathway to Restore Kidney Tissue from Cobalt-Mediated Oxidative Injury and Inflammation in Rats

“…Additionally, ROS can damage the cell membrane by reacting with the phospholipid moieties of the membrane polyunsaturated fatty acids, mediating lipid peroxidation. This was in accordance with the previous studies that demonstrated the CoCl 2 -induced oxidative injury in different body systems [11,53].…”

Environmental Exposures in the Etiology of Abortion: Placental Toxic and Trace Element Levels

“…Although it is well known that Co induces hypoxia by inhibiting proline hydroxylase in biologic systems, exact mechanisms for different toxicities in various organ systems have been studied. Increased use of Co, especially in orthopedic surgery and artificial manu- facturing, has caused cytotoxic, genotoxic, and immunologic effects in patients, and has led to the development of conditions such as pseudo-tumor, an aseptic lymphocytic vasculitis associated with high inflammation [52]. In our study, the detection of higher levels of Co in the SA group can be explained with the formation of a hypoxic and inflammatory process in the placental environment.…”

Novel antihypertensive action of rutin is mediated via inhibition of angiotensin converting enzyme/mineralocorticoid receptor/angiotensin 2 type 1 receptor (ATR1) signaling pathways in uninephrectomized hypertensive rats

“…The immunohistochemical expressions of angiotensin 2 type 1 receptor (ATR1), angiotensin converting enzyme (ACE), mineralocorticoid receptor (MCR), caspase 3 were evaluated in kidney and testes, respectively, using paraffin embedded tissues that were deparaffinized in xylene and rehydrated with graded alcohol. Antigen retriever, peroxidase quenching, blocking non‐specific binding, and overnight incubation with anti‐ATR1, anti‐ACE, anti‐caspase 3, and anti‐MCR primary antibodies were carried out as previously described (Oyagbemi et al., 2019). The immune‐positive reactions were enhanced with 3, 3′‐Diaminobenzidine (DAB; AMRESCO LLC.…”