Flaxseed oil ameliorates mercuric chloride-induced liver damage in rats

AlRamadneh, Tareq Nayef; Alqurashi, Naif; Khan, Mohd Sajjad Ahmad; Hashimi, Saeed Mujahid; Javaraiah, Rajesh; Al-Ostoot, Fares Hezam; Alhaija, Abed Alkarem Abu

doi:10.1016/j.jtemb.2022.126965

Cited by 6 publications

(5 citation statements)

References 37 publications

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“…Then, glutathione sulphate glutathione (GSSG) is created when glutathione (GSH) is reduced to glutathione (GSH) by glutathione reductase. Toxins accumulate when GPx activity is reduced, which increases oxidative stress (Fatima et al, 2021, AlRamadneh et al, 2022. According to the results of our research, cisplatin signi cantly decreased both GPx and GSH.…”

Section: Discussionsupporting

confidence: 54%

Protective Effects of Omega-3 Fatty Acids Against Cisplatin Induced Hepatocellular Damage and Oxidative Stress in Rats

ALRAMADNEH,

Abu-Harirah,

Saleh

et al. 2023

Preprint

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Cisplatin has a high rate of effectiveness in treating cancer, its use is restricted due to the severe adverse consequences it produces. Nephrotoxicity, neurotoxicity, and ototoxicity are only a few of the unwanted side effects. In the case of cisplatin, hepatotoxicity is thought to be caused by oxidative stress brought on by an increase in reactive oxygen species (ROS). Omega-3 is an antioxidant that reduces the production of reactive oxygen species by inhibiting the enzyme nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. This study aimed to compare the beneficial effects of omega-3 therapy against the harmful effects of cisplatin-induced hepatotoxicity and to determine the effect of cisplatin on hepatic pro-oxidant or antioxidant systems. The rats were divided into four groups (n = 6 per group) and treated with single dosages of cisplatin (5 milligrams per kilogram) and omega-3 (20 milligrams per kilogram over fourteen days by intraperitoneal administration), or cisplatin combined with omega-3. In addition, the rat’s blood was tested for alkaline phosphatase, aspartate transaminase, and alanine transaminase levels. We observed higher levels of lipid peroxidation products, total oxidant status, and ALT in the cisplatin group compared to the control group. Conversely, it was revealed that glutathione peroxidase and superoxide dismutase levels were considerably lower in the cisplatin group compared to the control group. Omega-3 has significantly reduced the toxicity of cisplatin in the liver. Our biochemical results confirmed our histological observations of central venous dilations, pericenter and periportal sinusoidal dilations, parenchymal inflammation, vacuolar abnormalities in hepatocytes, biliary duct proliferation, and caspase-3 positive hepatocytes. In conclusion, Omega-3 can provide biochemical and histological protection against cisplatin-induced hepatotoxicity.

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Section: Discussionsupporting

confidence: 54%

Protective Effects of Omega-3 Fatty Acids Against Cisplatin Induced Hepatocellular Damage and Oxidative Stress in Rats

ALRAMADNEH,

Abu-Harirah,

Saleh

et al. 2023

Preprint

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“…In a study reporting that mercury chloride leads to oxidative stress and consequently liver damage by triggering an increase in hydrogen peroxide formation, intensification of lipid peroxidation and glutathione depletion, it was shown that mercury chloride exposure triggered histopathologic changes such as congestion and portal area enlargement with perivascular leukocyte infiltration in the beginning, followed by intense fibrosis, degeneration, and necrosis in hepatocytes 48 . In addition, in another study, loss of liver morphology, interstitial edema and necrosis in hepatocytes were observed with mercury chloride exposure 49 . In addition, Kupffer cell hyperplasia with necrosis, pyknotic and hyperchromic nucleus and eosinophilization in hepatocytes, parenchymal hemorrhage and mononuclear cell infiltration in the portal region were observed in mercury chloride toxicity 37 .…”

Section: Discussionmentioning

confidence: 94%

“…48 In addition, in another study, loss of liver morphology, interstitial edema and necrosis in hepatocytes were observed with mercury chloride exposure. 49 In addition, Kupffer cell hyperplasia with necrosis, pyknotic and hyperchromic nucleus and eosinophilization in hepatocytes, parenchymal hemorrhage and mononuclear cell infiltration in the portal region were observed in mercury chloride toxicity. 37 Similarly, our results revealed the presence of histopathologic changes such as degeneration and necrosis in hepatocytes, karyolytic nucleus, Kupffer cell activation and mononuclear cell infiltration in the periportal region (Table 4, Figure 1).…”

Section: Discussionmentioning

confidence: 98%

Effects of naringenin on oxidative damage and apoptosis in liver and kidney in rats subjected to chronic mercury chloride

Kahramanoğullari,

Erişir,

Yaman

et al. 2024

Environmental Toxicology

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Mercury chloride is a type of heavy metal that causes the formation of free radicals, causing hepatotoxicity, nephrotoxicity and apoptosis. In this study, the effects of naringenin on oxidative stress and apoptosis in the liver and kidney of rats exposed to mercury chloride were investigated. In the study, 41 2‐month‐old male Wistar‐Albino rats were divided into five groups. Accordingly, group 1 was set as control group, group 2 as naringenin‐100, group 3 as mercury chloride, group 4 as mercury chloride + naringenin‐50, and group 5 as mercury chloride + naringenin‐100. For the interventions, 1 mL/kg saline was administered to the control, 0.4 mg/kg/day mercury (II) chloride to the mercury chloride groups by i.p., and 50 and 100 mg/kg/day naringenin prepared in corn oil to the naringenin groups by gavage. All the interventions lasted for 20 days. Mercury chloride administration was initiated 1 h following the administration of naringenin. When mercury chloride and the control group were compared, a significant increase in plasma urea, liver and kidney malondialdehyde (MDA) levels, in kidney superoxide dismutase (SOD), glutathione peroxidase (GSH‐Px), glutathione‐S‐transferase (GST) activities (p < .001), and a significant decrease in liver and kidney glutathione (GSH) levels (p < .001), in liver catalase (CAT) activity (p < .01) were observed. In addition, histopathological changes and a significant increase in caspase‐3 levels were detected (p < .05). When mercury chloride and treatment groups were compared, the administration of naringenin caused a decrease aspartate transaminase (AST), alanine transaminase (ALT), lactate dehydrogenase (LDH) (p < .01), urea, creatinine levels (p < .001) in plasma, MDA levels in liver and kidney, SOD, GSH‐Px, GST activities in kidney (p < .001), and increased GSH levels in liver and kidney. The addition of naringenin‐100 increased GSH levels above the control (p < .001). The administration of naringenin was also decreased histopathological changes and caspase‐3 levels (p < .05). Accordingly, it was determined that naringenin is protective and therapeutic against mercury chloride‐induced oxidative damage and apoptosis in the liver and kidney, and 100 mg/kg naringenin is more effective in preventing histopathological changes and apoptosis.

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“…When compared to antihyperlipidemic medications, the combination of flaxseed and fennel seed may play a significant role in enhancing liver function. In rats, AST and ALT were noticeably increased, and 6 weeks of anethole, SDG, combination, and atorvastatin treatment significantly decreased their levels (AlRamadneh et al, 2022 ). These findings were supported by a histological examination that showed all rats treated with anethole, SDG, their combination, and atorvastatin had liver tissues that seemed to have a normal histological structure (Figure 3 ).…”

Section: Discussionmentioning

confidence: 99%

Secoisolariciresinol diglucoside and anethole ameliorate lipid abnormalities, oxidative injury, hypercholesterolemia, heart, and liver conditions

Noreen

Rehman

Tufail

et al. 2023

Food Science & Nutrition

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Fennel seeds and flaxseed have been traditionally used against many medical ailments due to their medicinal characteristics. The aim of the study was to investigate the health properties of secoisolariciresinol diglucoside (SDG) and anethole from flaxseed and fennel seeds in rats fed with high‐fat diet. Histopathological changes in the heart and liver were also examined. Sixty rats were divided into two main groups. Group I (10 rats) was used as a negative control group and fed on the basal diet only. Group II (50 rats) was fed a hypercholesterolemic diet but not given any drugs during the trial for 2 weeks. This group was further divided into five subgroups (10 rats each). One of them was fed on the basal diet and used as a positive control group. However, the other four subgroups were fed on basal diets and anethole (20 mg/kg/day, orally), SDG (20 mg/kg/day, orally), a mixture of anethole + SDG (10 + 10 mg/kg/day, orally), and atorvastatin (10 mg/kg/day, orally) for 6 weeks. Compared to control, treatment with a combination of anethole + SDG showed a significant (p ≤ .05) improvement in serum levels of triglyceride (TG) (137.88 ± 1.61 mg/dL), total cholesterol‐(TC) (180.12 ± 8.99 mg/dL), LDL‐C (46.40 ± 6.67 mg/dL), VLDL‐C (11.81 ± 1.07 mg/dL), aspartate aminotransferase (AST) (75.97 ± 6.92 U/L), alanine aminotransferase (ALT) (34.83 ± 2.17 U/L), alkaline phosphatase (ALP) (130.65 ± 1.05 U/L), and malondialdehyde (MDA) (30.12 ± 1.89 mmol/g), and improved activities of catalase (70.99 ± 3.29 U/g) and superoxide dismutase (SOD) (35.13 ± 2.53 U/dL) enzymes while SDG and anethole group had relatively less impact. Atorvastatin also improved serum levels of triglyceride, total cholesterol, LDL‐C, and VLDL‐C significantly and rose serum high‐density lipoprotein cholesterol (HDL‐C) levels considerably meanwhile it had a minor but negative impact on AST, ALT, and ALP, and negligible impact on activities of MDA, CAT, and SOD enzymes compared to the positive control group. The study revealed that combining anethole and SDG may improve dyslipidemia, improve lipid profile, decrease risks of chronic heart diseases, increase HDL‐C, and enhance antioxidant enzymes' activities.

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Flaxseed oil ameliorates mercuric chloride-induced liver damage in rats

Cited by 6 publications

References 37 publications

Protective Effects of Omega-3 Fatty Acids Against Cisplatin Induced Hepatocellular Damage and Oxidative Stress in Rats

Protective Effects of Omega-3 Fatty Acids Against Cisplatin Induced Hepatocellular Damage and Oxidative Stress in Rats

Effects of naringenin on oxidative damage and apoptosis in liver and kidney in rats subjected to chronic mercury chloride

Secoisolariciresinol diglucoside and anethole ameliorate lipid abnormalities, oxidative injury, hypercholesterolemia, heart, and liver conditions

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