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المؤلفAzza, Naija
المؤلفYalcin, Huseyin Cagatay
تاريخ الإتاحة2023-04-30T08:09:01Z
تاريخ النشر2023-12-31
اسم المنشورToxicology Reports
المعرّفhttp://dx.doi.org/10.1016/j.toxrep.2023.04.009
الاقتباسNaija, Azza, and Huseyin Cagatay Yalcin. "EVALUATION OF CADMIUM AND MERCURY ON CARDIOVASCULAR AND NEUROLOGICAL SYSTEMS: EFFECTS ON HUMANS AND FISH." Toxicology Reports (2023).
الرقم المعياري الدولي للكتاب22147500
معرّف المصادر الموحدhttps://www.sciencedirect.com/science/article/pii/S2214750023000458
معرّف المصادر الموحدhttp://hdl.handle.net/10576/42152
الملخصChemicals are at the top of public health concerns and metals have received much attention in terms of toxicological studies. Cadmium (Cd) and mercury (Hg) are among the most toxic heavy metals and are widely distributed in the environment. They are considered important factors involved in several organ disturbances. Heart and brain tissues are not among the first exposure sites to Cd and Hg but they are directly affected and may manifest intoxication reactions leading to death. Many cases of human intoxication with Cd and Hg showed that these metals have potential cardiotoxic and neurotoxic effects. Human exposure to heavy metals is through fish consumption which is considered as an excellent source of human nutrients. In the current review, we will summarize the most known cases of human intoxication with Cd and Hg, highlight their toxic effects on fish, and investigate the common signal pathways of both Cd and Hg to affect heart and brain tissues. Also, we will present the most common biomarkers used in the assessment of cardiotoxicity and neurotoxicity using Zebrafish model.
راعي المشروعThe open-access finding of the present work is provided by the Qatar National Library (QATAR).
اللغةen
الناشرElsevier
الموضوعCadmium
Mercury
Fish
Humans
Heart
Brain
العنوانEvaluation of cadmium and mercury on cardiovascular and neurological systems: Effects on humans and fish
النوعArticle
الصفحات498-508
رقم المجلد10
Open Access user License http://creativecommons.org/licenses/by/4.0/
dc.accessType Open Access


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