Oxidative Effects of Potassium Dichromate on Biochemical, Hematological Characteristics, and Hormonal Levels in Rabbit Doe (Oryctolagus cuniculus)

Momo, Chongsi Margaret Mary; Ferdinand, Ngoula; Bebe, Ngouateu Kenfack Omer; Marquise, Makona Ndekeng Alexane; Kenfack, Augustave; Narcisse, Vemo Bertin; Hervé, Tchoffo; Tchoumboué, J.

doi:10.3390/vetsci6010030

Cited by 21 publications

(6 citation statements)

References 44 publications

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“…The uptake of Cr (VI) increased the plasma activities of AST and ALT, while a concomitant decrease of these enzymes in the liver was also observed, indicating hepatic damage. This observation was previously reported in mice, rats, and rabbits (33)(34)(35). The increase of these enzyme activities could be as a result of Cr (VI) induced oxidative stress hepatic damage releasing the enzymes from the cytoplasm of hepatocytes into the plasma (36).…”

Section: Discussionsupporting

confidence: 80%

Potassium Dichromate-Induced Hepato- and Hematotoxicity in Rats: Nutritive Composition and Ameliorative Role of Acacia nilotica L. Leaf

Ejoh

Iheagwam

Olusola

2021

Jundishapur J Nat Pharm Prod

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Background: Chromium and its salts, as well as chromium-containing compounds, play a major role in numerous manufacturing processes and have been contraindicated in carcinogenic, toxic, and mutagenic conditions in people involved in these processes. Objectives: This study investigated the ameliorative role of Acacia nilotica aqueous leave extract (ANLA) on potassium dichromate-induced liver and blood toxicity in male and female rats. Phytochemical screening and nutrient composition of ANLA were also evaluated. Methods: Phytochemical and proximate analysis of ANLA were carried out. Twenty adult male and female rats each were divided into four groups (n = 10): (1) control; (2) potassium dichromate (PDC; 0.625 mg/kg body weight); (3) PDC co-treated with ANLA after seven days (650 mg/kg bwt); and (4) PDC co-treated with ANLA (650 mg/kg bwt) simultaneously for 21 days. Biomarkers of liver injury, lipid, and hematological imbalance were assessed. Tissue histology and toxicant retention were done. Results: Various plant secondary metabolites (flavonoids, terpenoids, tannins, phenols, saponins, cardiac glycosides, alkaloids, and anthraquinones) and nutrients (protein = 67.41 ± 2.44%; carbohydrate = 9.87 ± 1.87%; fiber = 10.01 ± 1.21%; mineral = 6.41 ± 1.08%; fat and oil = 6.63 ± 0.93%) were identified in the leave. Exposure to chromium significantly (P < 0.05) increased plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) with a concomitant decrease in the activity of these enzymes in the liver of both male and female rats. The exposure also altered protein, triglyceride, and cholesterol levels in the plasma and liver as well as hematological indices. Organ chromium retention and pathological changes were also observed. ANLA modulated these chromium-induced alterations in the rats. Conclusions: Based on the results, ANLA indicates ameliorative property against PDC-induced toxicity in rats. Thus it may be used to combat chromium poisoning. The nutritive potential of A. nilotica leaves may also be maximized.

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Section: Discussionsupporting

confidence: 80%

Potassium Dichromate-Induced Hepato- and Hematotoxicity in Rats: Nutritive Composition and Ameliorative Role of Acacia nilotica L. Leaf

Ejoh

Iheagwam

Olusola

2021

Jundishapur J Nat Pharm Prod

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“…GSH is known to protect cells from the toxic effects of lipid peroxidation. Furthermore, GSH is essential to maintain cellular redox status and its consumption is considered to be an indicator of oxidative stress ( 41 ). GSH-Px can promote the breakdown of H 2 O 2 and reduce toxic peroxides to nontoxic hydroxyl compounds, thereby protecting the structure and function of the cellular membrane from oxide damage.…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin gallate enhances human lens epithelial cell survival after UVB irradiation via the mitochondrial signaling pathway

Song

Gao

et al. 2022

Mol Med Rep

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“…Some researchers believe that oxidative stress with the formation of ROS and activation of apoptosis resulting from mitochondrial dysfunction is a key link in the degeneration of retinal ganglion cells and their axons in the optic nerve [24,25]. According to the literature, Cr (VI) enhances the accumulation of ROS by blocking complex I of the mitochondrial respiratory chain [26], and also reduces the activity of antioxidant enzymes [27]. Cr (VI), like other cationic metals, penetrates the outer mitochondrial membrane through the mechanism of molecular mimicry [28,29].…”

Section: Discussionmentioning

confidence: 99%

RESEARCH OF REPARATIVE MECHANISMS IN THE OPTIC NERVE IN TOXIC NEUROPATHY CAUSED BY Cr (VI)

2020

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Intoxication lesions of the optic nerve (toxic optic neuropathy, TON) most often occur under the influence of exogenous factors, including heavy metals. Сell survival under stress have involves heat shock proteins (HSPs). The aim of the research. To assess the optic nerve’s immunoreactivity to heat shock proteins of the HSP70 and HSP90α families and reveal its relationship with the severity of morphological changes in toxic optic neuropathy caused by Cr (VI). Materials and methods. The study was conducted on 48 mature male rats. The experimental groups were given to drink water with Cr(VI) for 20, 40 and 60 days. This type of water is typical for the water basins in the northern districts of the Sumy region. Optic nerves сhanges under the influence of Cr(VI) have investigated by the morphometric method. Neuroglial cells and capillary endothelial cells were assessed by immunohistochemistry by HSP70α and HSP90 expression for intensity and spatial distribution. Results. The data analysis revealed that Cr (VI) has a neurotoxic effect on the optic nerve with the development of edema, which is manifested by the thickening of nerve fibers. The dynamics of HSP70 immunoexpression in the endothelium of the optic nerve capillaries of rats on 20 and 40 experimental days was characterized by stable values and was 1.5 times higher than the control. The maximum number of positively stained cells for the HSP70 marker was detected in endothelial cells of the microvasculature for 60 days – 82.44±12.42 %. HSP70 levels in neuroglia cells of optic nerve have decreased on day 40 (55.66±11.56% p=0.05) and lower than the control (70.44±4.81 %.) group. Optic nerve capillaries was highest immunoactivity on HSP90 in group II endothelial cells – 51.22±14.57% (p=0.05). The activity of HSP90α protein in optic neuroglia cells was characterized by a gradual increase in the duration of the experiment and was higher by 12, 4 % in experimental group III (81.77±21.67 %) compared with control (71.66±4.95 %). Conclusions. Our study provides an insight into the significant difference in the immunoreactivity of heat shock proteins of the HSP70 and HSP90α families in neuroglia and endothelial cells of the optic nerve capillaries under the influence of Cr(VI). The results obtained suggest that Cr (VI) has a neurotoxic effect on the optic nerve with the development of edema, which is manifested by the thickening of nerve fibers. A comparison of the dynamics of the development of the dystrophic process in the optic nerve with the results of the immunohistochemical analysis showed, that an increase in the thickness of nerve fibers is accompanied by an increase in immunoreactive neuroglial cells (HSP90α) and endothelial cells (HSP70).

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Oxidative Effects of Potassium Dichromate on Biochemical, Hematological Characteristics, and Hormonal Levels in Rabbit Doe (Oryctolagus cuniculus)

Cited by 21 publications

References 44 publications

Potassium Dichromate-Induced Hepato- and Hematotoxicity in Rats: Nutritive Composition and Ameliorative Role of Acacia nilotica L. Leaf

Potassium Dichromate-Induced Hepato- and Hematotoxicity in Rats: Nutritive Composition and Ameliorative Role of Acacia nilotica L. Leaf

Epigallocatechin gallate enhances human lens epithelial cell survival after UVB irradiation via the mitochondrial signaling pathway

RESEARCH OF REPARATIVE MECHANISMS IN THE OPTIC NERVE IN TOXIC NEUROPATHY CAUSED BY Cr (VI)

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