<i>In vivo</i> genotoxicity and cytotoxicity assessment of a novel quinoxalinone with trichomonacide activity

Rivera, Norma; Rojas, Marcela; Zepeda, Armando; Malagón, Filiberto; Arán, Vicente J.; Marrero-Ponce, Yovani; Rivera, Ernesto; Fortoul, Teresa I.

doi:10.1002/jat.2819

Cited by 6 publications

(1 citation statement)

References 32 publications

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“…28 The use of an in vivo approach makes it easier to understand how various medications, chemicals, and known environmental contaminants affect animals, not only at the cellular and tissue levels but also with regard to the intricate metabolic processes occurring across the animal's many tissues. Innumerable studies on genotoxicity have been conducted using mice 29,30 and rats. 31.32 However, since many animals must be used and a lot of test substances have to be employed, in vivo models wind up being highly expensive.…”

Section: Introductionmentioning

confidence: 99%

Bio-Evaluation, In-Vitro and In-Vivo Anti-Inflammatory Activity, Therapeutic Efficacy, and Genotoxicity of the Potentials of the Green Seaweed Valoniopsis Pachynema using Zebra Fish Larvae (Danio Rerio) as an Animal Model

Bhuvaneshwari.¹,

P²

2023

Pharmacogn J.

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major component of the host's defense against many harmful agents, such as the invasion of foreign pathogens, physical injury, and other hostile immunological reactions, is regarded to be inflammation in general. 2,3 However, persistent, arthritis, rheumatoid, asthma, multiple sclerosis, inflammatory bowel disease, diabetes, cancer and psoriasis are only a few of the disorders that can be triggered by excessive or protracted inflammation. 4 Among these diseases, Psoriasis is one of the most frequent non-pathogenic skin conditions that have been identified so far. Psoriasis is a complex and multifaceted chronic inflammatory skin disease brought on by a confluence of hereditary and environmental factors. 5 About 2-3% of the inhabitants worldwide have psoriasis. Psoriasis is characterised by telangiectasia in the dermal papillae, hyperproliferation of keratinocytes, and recruitment of inflammatory cells to the epidermis. 6 Psoriasis is said to be caused because of the traumatic, environmental, or pharmacological stimuli that cause abnormal interaction among keratinocytes and various types of immune cell, results in exposed increase of pro-proliferative and inflammatory circuits in susceptible individuals. Certain clinical symptoms associated with this disorder are plaque, psoriasis, inverse psoriasis, Psoriasis vulgaris, palmoplantar psoriasis, erythrodermic psoriasis, pustular psoriasis and scalp psoriasis. [7][8][9][10] The entire skin surface of the body can also be affected. 11 Normal skin has a 30-day life cycle, but psoriasis has a 1.5-3-day life cycle. Nails and skin are frequently affected by psoriasis. Patients with psoriasis may also have concomitant conditions such as obesity, psoriatic arthritis, diabetes, metabolic syndrome, and cardiovascular diseases. 12 Consequently, it is also referred to as a T-cell mediated autoimmune illness. Interleukins (ILs), tumour necrosis factor (TNF-), and interferon-(IFN-) levels of inflammatory cytokines increase modestly in systemic circulation, but mostly in the dermis. Vascular-Endothelial Growth-Factor (VEGF) is created by mast cells, keratinocytes, and macrophages as a result of elevated levels of cytokines and other inflammatory mediators. New blood vessels are created as a result, increasing blood flow. According to recent research, there are 25 genetic variations that cause psoriasis. The cause of psoriasis is immune system activation, and the psoriasiscausing gene has been found. This could give precise and effective treatments to treat psoriasis. 13

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Section: Introductionmentioning

confidence: 99%

Bio-Evaluation, In-Vitro and In-Vivo Anti-Inflammatory Activity, Therapeutic Efficacy, and Genotoxicity of the Potentials of the Green Seaweed Valoniopsis Pachynema using Zebra Fish Larvae (Danio Rerio) as an Animal Model

Bhuvaneshwari.¹,

P²

2023

Pharmacogn J.

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Antimalarial efficacy, cytotoxicity, and genotoxicity of methanolic stem bark extract from Hintonia latiflora in a Plasmodium yoelii yoelii lethal murine malaria model

et al. 2014

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Traditional medicines have been used to treat malaria for thousands of years and are the source of artemisinin and quinine derivatives. With the increasing levels of drug resistance, the high cost of artemisisnin-based combination therapies, and fake antimalarials drugs, traditional medicine have become an important and sustainable source of malaria treatment. For the benefit of those who use traditional medicine to treat malaria, there is an urgent need to study the efficacy and toxicity of herbal remedies. Hintonia latiflora stem bark infusions are use in Mexican traditional medicine to treat malaria, diabetes, and gastrointestinal diseases. Its efficacy in the treatment of complicated malaria and its ability to generate DNA damage to the host is not fully evaluated. In our search for antimalarial natural products, in the present study, we tested the efficacy of H. latiflora stem bark methanolic extract (HlMeOHe) in CD1 male mice infected with lethal Plasmodium yoelii yoelii and its in vivo cytotoxicity and genotoxicity. To assess the antimalarial activity, the extract was evaluated in a 4-day test scheme in oral doses of 1,200, 600, and 300 mg/kg prior acute toxicity test; oral chloroquine (15 mg/kg) was used as positive control. The ability of 1,200 mg/kg of HlMeOHe to induce cytotoxicity and DNA damage in the peripheral blood of mice was assessed using a fluorochrome-mediated viability test and the micronucleus (MN) assay; N-ethyl-N-nitrosourea (ENU) was used as a positive control. HlMeOHe median acute toxicity (LD₅₀) was 2,783.71 mg/kg and LD10 was 1,293.76 mg/kg (taken as the highest work dose). Plasmodium yoelii yoelii-infected mice in the untreated control group died between 6 and 7 days post-infection (PI) with parasitemia over 70%. Even though mice treated with 600 and 300 mg/kg showed a chemosuppression percentage of total parasitemia of 99.23 and 23.66, respectively, animals in both groups died 6 to 7 days PI with parasitemia over 45%. A 4-day dosage of 1,200 mg/kg of the extract showed, in the P. yoelii yoelii-infected mice, a 100% chemosuppression of total parasitemia on 5 days PI and a 23 days survival time with a mean parasitemia of 23.6% at the date of death. Only mice treated with chloroquine survived until the end of the experiment. Cell viability was not affected. The average number of micronuclei in the treated mice increased significantly (P < 0.05) to 4.8 MN when compared with the untreated control group (0.9 MN). The results obtained in this study showed that the infection outcome of P. yoelii yoelii-infected mice is affected by HlMeOHe. Although a concentration of 1,200 mg/kg of HlMeOHe is suitable to use in the treatment of malaria fever, slowed down the parasite replication, retarded the patency time, and increased the infected P. yoelii yoelii mice survival time, its chemical composition should be studied in detail in order to reduce its genotoxic potential.

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Molecular docking and dynamic simulations of quinoxaline 1,4-di-N-oxide as inhibitors for targets from Trypanosoma cruzi, Trichomonas vaginalis, and Fasciola hepatica

et al. 2023

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In vivo genotoxicity and cytotoxicity assessment of a novel quinoxalinone with trichomonacide activity

Cited by 6 publications

References 32 publications

Bio-Evaluation, In-Vitro and In-Vivo Anti-Inflammatory Activity, Therapeutic Efficacy, and Genotoxicity of the Potentials of the Green Seaweed Valoniopsis Pachynema using Zebra Fish Larvae (Danio Rerio) as an Animal Model

Bio-Evaluation, In-Vitro and In-Vivo Anti-Inflammatory Activity, Therapeutic Efficacy, and Genotoxicity of the Potentials of the Green Seaweed Valoniopsis Pachynema using Zebra Fish Larvae (Danio Rerio) as an Animal Model

Antimalarial efficacy, cytotoxicity, and genotoxicity of methanolic stem bark extract from Hintonia latiflora in a Plasmodium yoelii yoelii lethal murine malaria model

Molecular docking and dynamic simulations of quinoxaline 1,4-di-N-oxide as inhibitors for targets from Trypanosoma cruzi, Trichomonas vaginalis, and Fasciola hepatica

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