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JournalISSN: 1687-8191

Journal of Toxicology 

Hindawi Publishing Corporation
About: Journal of Toxicology is an academic journal published by Hindawi Publishing Corporation. The journal publishes majorly in the area(s): Oxidative stress & Apoptosis. It has an ISSN identifier of 1687-8191. It is also open access. Over the lifetime, 436 publications have been published receiving 11916 citations.


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Journal ArticleDOI
TL;DR: The nature of ROS-induced damage on key cellular targets of oxidative stress is examined and evidence implicating ROS in clinically relevant, drug-related side effects including doxorubicin-induced cardiac damage, azidothymidine-induced myopathy, and cisplatin-induced ototoxicity is reviewed.
Abstract: Reactive oxygen species (ROS) are a byproduct of normal metabolism and have roles in cell signaling and homeostasis. Species include oxygen radicals and reactive nonradicals. Mechanisms exist that regulate cellular levels of ROS, as their reactive nature may otherwise cause damage to key cellular components including DNA, protein, and lipid. When the cellular antioxidant capacity is exceeded, oxidative stress can result. Pleiotropic deleterious effects of oxidative stress are observed in numerous disease states and are also implicated in a variety of drug-induced toxicities. In this paper, we examine the nature of ROS-induced damage on key cellular targets of oxidative stress. We also review evidence implicating ROS in clinically relevant, drug-related side effects including doxorubicin-induced cardiac damage, azidothymidine-induced myopathy, and cisplatin-induced ototoxicity.

542 citations

Journal ArticleDOI
TL;DR: The biosorption capacity with respect to the use of bacteria, fungi, biofilm, algae, genetically engineered microbes, and immobilized microbial cell for the removal of heavy metals is discussed.
Abstract: The discharge of untreated tannery wastewater containing biotoxic substances of heavy metals in the ecosystem is one of the most important environmental and health challenges in our society. Hence, there is a growing need for the development of novel, efficient, eco-friendly, and cost-effective approach for the remediation of inorganic metals (Cr, Hg, Cd, and Pb) released into the environment and to safeguard the ecosystem. In this regard, recent advances in microbes-base heavy metal have propelled bioremediation as a prospective alternative to conventional techniques. Heavy metals are nonbiodegradable and could be toxic to microbes. Several microorganisms have evolved to develop detoxification mechanisms to counter the toxic effects of these inorganic metals. This present review offers a critical evaluation of bioremediation capacity of microorganisms, especially in the context of environmental protection. Furthermore, this article discussed the biosorption capacity with respect to the use of bacteria, fungi, biofilm, algae, genetically engineered microbes, and immobilized microbial cell for the removal of heavy metals. The use of biofilm has showed synergetic effects with many fold increase in the removal of heavy metals as sustainable environmental technology in the near future.

496 citations

Journal ArticleDOI
TL;DR: Emerging evidence suggests that air pollution-induced neuroinflammation, oxidative stress, microglial activation, cerebrovascular dysfunction, and alterations in the blood-brain barrier contribute to CNS pathology.
Abstract: Exposure to ambient air pollution is a serious and common public health concern associated with growing morbidity and mortality worldwide. In the last decades, the adverse effects of air pollution on the pulmonary and cardiovascular systems have been well established in a series of major epidemiological and observational studies. In the recent past, air pollution has also been associated with diseases of the central nervous system (CNS), including stroke, Alzheimer's disease, Parkinson's disease, and neurodevelopmental disorders. It has been demonstrated that various components of air pollution, such as nanosized particles, can easily translocate to the CNS where they can activate innate immune responses. Furthermore, systemic inflammation arising from the pulmonary or cardiovascular system can affect CNS health. Despite intense studies on the health effects of ambient air pollution, the underlying molecular mechanisms of susceptibility and disease remain largely elusive. However, emerging evidence suggests that air pollution-induced neuroinflammation, oxidative stress, microglial activation, cerebrovascular dysfunction, and alterations in the blood-brain barrier contribute to CNS pathology. A better understanding of the mediators and mechanisms will enable the development of new strategies to protect individuals at risk and to reduce detrimental effects of air pollution on the nervous system and mental health.

489 citations

Journal ArticleDOI
TL;DR: As vehicular traffic is known to importantly contribute to PM exposure, its intensity and quality must be strongly relevant determinants of the qualitative characteristics of PM spread in the atmosphere.
Abstract: Air pollution is associated with increased cardiovascular and pulmonary morbidity and mortality. The mechanisms of air pollution-induced health effects involve oxidative stress and inflammation. As a matter of fact, particulate matter (PM), especially fine (PM2.5, PM < 2.5 μm) and ultrafine (PM0.1, PM < 0.1 μm) particles, ozone, nitrogen oxides, and transition metals, are potent oxidants or able to generate reactive oxygen species (ROS). Oxidative stress can trigger redox-sensitive pathways that lead to different biological processes such as inflammation and cell death. However, it does appear that the susceptibility of target organ to oxidative injury also depends upon its ability to upregulate protective scavenging systems. As vehicular traffic is known to importantly contribute to PM exposure, its intensity and quality must be strongly relevant determinants of the qualitative characteristics of PM spread in the atmosphere. Change in the composition of this PM is likely to modify its health impact.

488 citations

Journal ArticleDOI
TL;DR: A brief summary of heavy metals homeostasis is given, followed by a description of the available evidence for their link with CVD and the proposed mechanisms of action by which their toxic effects might be explained, and suspected interactions between genetic, nutritional and environmental factors are discussed.
Abstract: Cardiovascular disease (CVD) is an increasing world health problem. Traditional risk factors fail to account for all deaths from CVD. It is mainly the environmental, dietary and lifestyle behavioral factors that are the control keys in the progress of this disease. The potential association between chronic heavy metal exposure, like arsenic, lead, cadmium, mercury, and CVD has been less well defined. The mechanism through which heavy metals act to increase cardiovascular risk factors may act still remains unknown, although impaired antioxidants metabolism and oxidative stress may play a role. However, the exact mechanism of CVD induced by heavy metals deserves further investigation either through animal experiments or through molecular and cellular studies. Furthermore, large-scale prospective studies with follow up on general populations using appropriate biomarkers and cardiovascular endpoints might be recommended to identify the factors that predispose to heavy metals toxicity in CVD. In this review, we will give a brief summary of heavy metals homeostasis, followed by a description of the available evidence for their link with CVD and the proposed mechanisms of action by which their toxic effects might be explained. Finally, suspected interactions between genetic, nutritional and environmental factors are discussed.

336 citations

Performance
Metrics
No. of papers from the Journal in previous years
YearPapers
20232
20221
202125
202035
201925
201839