Copper(I)-Nicotinic Acid Complex: An Immunopotentiator in Chickens Vaccinated Against Newcastle Disease

Musa, Sanjin; Hafez, Ali A. Abdel; Nassar, Ahmed; Gohar, M. A.

doi:10.1007/978-1-4612-4584-1_26

Cited by 4 publications

(3 citation statements)

References 6 publications

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“…This complex showed a pharmaceutical activity against Newcastle disease (Musa et al, 1987), anti-inflammatory effect against drastic induced rat model for gastric ulcer (el-Saadani et al, 1993), reduction of adverse effects of 5-fluorouracil in HCC persons (El-Saadani, 2004), prophylactic effect against induction of fatty liver in rats (Salama et al, 2007) as well as curative effect against induced rat burn skin injury (Nassar et al, 2012). Previously this Cu + -nicotinic acid complex was tested as a potent antagonist in induced aflatoxicated rats (Shatat et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Copper (I)-Nicotinate Promotes Gene Expression of CYPs that Produce M1 and Q1 in Aflatoxicosed Rats

Salah¹,

Mostafa²,

Saleem³

et al. 2020

American Journal of Biochemistry and Biotechnology

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Aflatoxin-contaminated food poses a serious risk to both human and animal health. Copper (1)-nicotinate (Cu +-nicotinate) complex potentiated the prophylactic effect against chronic aflatoxicosis in the experimental animals through the synthesis of less toxic metabolites M1 and Q1 which are easily excreted in urine. To investigate the action of the safety Cu +-nicotinate complex on gene expression of Cytochrome 450 (CYP450) system, the liver tissue samples of orally administered rats for 3 weeks with aflatoxin B1 (AFB1; 30 µg/kg body weight), with and without association of the copper complex (400 µg/kg body weight) were assayed for their gene expression of CYP450 families including 1A2, 3A2 and 2C11 as well as histopathological examination of the hepatic tissue samples was performed. The obtained data denoted that the Cu +-nicotinate complex significantly reduced gene expression of CYP2C11 and CYP3A2 that enhancing the most toxic epoxide metabolite. On the contrary, this complex enhanced the expression of CYP1A2 that synthesize the less toxic metabolite M1 and Q1. The histopathological examination mostly confirmed such observation as the signs of aflatoxicosis were absent in Cu +-nicotinate-treated group. Consequently, it could be predicted that the Cu +-nicotinate complex may be medically used as an inhibitory food additive agent against exposure of aflatoxicosis in the intact animals since the complex contains the copper and nicotinic acid, the two daily required biochemical elements for sustaining live in healthy conditions.

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Section: Introductionmentioning

confidence: 99%

Copper (I)-Nicotinate Promotes Gene Expression of CYPs that Produce M1 and Q1 in Aflatoxicosed Rats

Salah¹,

Mostafa²,

Saleem³

et al. 2020

American Journal of Biochemistry and Biotechnology

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“…Antioxidants were now used to scavenge reactive oxygen species (ROS) inhibit advanced glycation end-products (AGEs) formation and used widely as additives in food industry for such purpose [16] . Copper (I) -Nictitate figure (2) was known for its antioxidant activity and therapeutic uses as anti-inflammatory in modulating gastric ulcer [17] , Newcastle diseases [18] , reducing hepatotoxicity of 5-Fluorouracil [19] and besides its effectiveness in preventing fatty liver in experimental animals [20] . The present study was designed to evaluate the effectiveness of Cu(I) Nicotinic acid complex in antagonizing AA induced hepatotoxicity in rat based on evidences provided by biochemical ,cell line culture cancer of Cu(l) Nictitate complex and histological study of liver tissue.…”

Section: Introductionmentioning

confidence: 99%

Copper (I) Nicotinate complex Abrogates Acrylamide Induced Hepatotoxicity in Male Rats: Biochemical and Histological Studies

El-Sawi

Aldajani

Mohamed

et al. 2019

IJFNS

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This study was conducted as a trail to abrogates acrylamide induced hepatotoxicity in male rats by administration of copper (I) nicotinic acid complex. Animals were divided into 4 groups ;GI: control kept on balanced diet and tap water , GII: Acrylamide group received acrylamide in drinking water (7.5 mg/kg b.w.) for 30 days. GIII: treated with copper (I)-nicotinate complex (400 μg/kg b.w.) after acrylamide intoxication for 30 days and GIV the complex then acrylamide (prophylactic). Results showed significant increase in serum levels of AST, ALT, ALP, GGT and total antioxidant capacity (TAC) in acrylamide group. Moreover a significant increase in tumer markers AFU and TNF-Alpha. while Levels of each of S. total protein and S. albumin were significantly decreased in ACR group compared with control. Histological study showed congestion of central vein in liver section and vacuolation of hepatocytes in ACR group. Anticancer activity using in-vitro cytotoxic assay of Cu (I) Nicotinate complex ; proves the anticancer properties of it comparing with doxorubicin. Treatment with Copper (I)-Nicotinate Complex restored tissue and serological indices concomitantly towards normal levels. These results revealed that Copper (I)-Nicotinate Complex is able to significantly alleviate the hepatotoxicity induced by AA in rats and could be utilized as a potent food additives.

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“…Generally, antioxidants may impact their anti-carcinogenic property by inducing cellular detoxification pathway [14, *Address correspondence to this author at the Al-Azhar University, Assiut Branch, Faculty of Science, Chemistry Department, Egypt; Tel: 00201006785228; E-mail : ahmedshatat82@yahoo.com 15]. With regard to many of the biologically active copper chelating complexes [16] was the copper (I)-nicotinate that exhibiting antioxidant activity as well as therapeutic pharmaceutical activity against Newcastle diseases [17], anti-inflammatory effect on gastric ulcer [18], reduction of adverse effects of 5-Fluorouracil in patients with hepatocelluler carcinoma [19] and curative effect against induction of fatty liver in experimental animals [20].…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Copper (I)-Nicotinate Complex Against Aflatoxicosis

R.¹

2013

TOTOXIJ

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Aflatoxicosis mostly leads to serious clinical signs of malnutrition, growth retardation, and impairment of utilization of nutrients, immunosupression, liver diseases and cancer. Detoxification or prevention of such toxicity is interesting to researchers in change field. In pursuit for an approach, the synthetic copper(I)-nicotinate complex has been evaluated against the traditional Butylated hydroxy toluene (BHT) for possible protective effects as a food additive in induced aflatoxicosed animals. Induction of toxicity in adult rats by AFB 1 60 µg/kg body weight divided on three times a week for consecutive five weeks resulted in marked hepatic necrosis, collagen fibers around portal tract and iron deposits as well as features of general cellular collapse and cirrhosis. The protective effects were tested on two animal groups by associate doses of BHT (0.05 mg / kg B.W.) in one group and copper (I) nicotinate complex (0.4 mg/kg B.W.) in the other. Results showed, in both groups, almost normal histological as well as biochemical markers especially those treated with the copper complex, which suggests that anti-inflammatory copper complex can be used as a protective agent against aflatoxicosis when used in doses resemble those used in pharmaceutical vitamin supplements.

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Copper(I)-Nicotinic Acid Complex: An Immunopotentiator in Chickens Vaccinated Against Newcastle Disease

Cited by 4 publications

References 6 publications

Copper (I)-Nicotinate Promotes Gene Expression of CYPs that Produce M1 and Q1 in Aflatoxicosed Rats

Copper (I)-Nicotinate Promotes Gene Expression of CYPs that Produce M1 and Q1 in Aflatoxicosed Rats

Copper (I) Nicotinate complex Abrogates Acrylamide Induced Hepatotoxicity in Male Rats: Biochemical and Histological Studies

Protective Effects of Copper (I)-Nicotinate Complex Against Aflatoxicosis

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