Protective role of Centella asiatica on lead-induced oxidative stress and suppressed reproductive health in male rats

2011 ◽  
Vol 32 (2) ◽  
pp. 146-154 ◽  
Author(s):  
S.B. Sainath ◽  
R. Meena ◽  
Ch. Supriya ◽  
K. Pratap Reddy ◽  
P. Sreenivasula Reddy
2012 ◽  
Vol 26 (12) ◽  
pp. 522-532 ◽  
Author(s):  
Suganya Sekaran ◽  
Selvakumar Kandaswamy ◽  
Krishnamoorthy Gunasekaran ◽  
Elumalai Perumal ◽  
Fariya Yasmine Afsar Basha ◽  
...  

2020 ◽  
Vol 7 (1) ◽  
pp. 140-154
Author(s):  
Zina Bouteraa ◽  
Rachid Rouabhi ◽  
Fouad Menaceur ◽  
Salim Gasmi

AbstractDuring recent years the defensive role of diferuloylmethane against oxidative stress and apoptosis has been experimentally documented. Fe3O4-NPs can cause cellular death by inducing oxidative stress. Present study aimed to investigate whether diferuloylmethane could protect rats mitochondria against Fe3O4-NPs intoxication. Twenty adult male rats were randomly chosen and divided into four groups: control; treated with 10 mg/kg/d of Fe3O4-NPs; treated with diferuloylmethane at the dose 20 ml/kg/d; treated with Fe3O4-NPs (10 mg/kg/d) and diferuloylmethane (20 ml/kg/d) respectively for 28 days. The results showed that Fe3O4-NPs increased the Alanine aminotransferase (ALT), aspartate aminotransferase (AST), lipid peroxidation, mit-GSH (Glutathione), mit-CAT (Catalase), mit-GST (Glutathione S-transferase) and decreased mit-GPx (Glutathione peroxidase), with increased in mitochondrial swelling and permeability followed by the increasing level of plasmatic Cyt-c. The addition of diferuloylmethane (DFM) to these samples reduces or corrects the amount of the most of biomarkers. These findings have demonstrated that DFM can act as an antioxidant and antiapoptotic factor against damages induced by Fe3O4-NPs.


2017 ◽  
Vol 95 (4) ◽  
pp. 1581-1595
Author(s):  
IBRAHIM H. BORAI ◽  
AZZA A. ATEF ◽  
AFAF A. EL KASHOUR ◽  
MAHMOUD M. SAID ◽  
RANIA A. MOHAMED

2010 ◽  
Vol 62 (1) ◽  
pp. 75-82 ◽  
Author(s):  
Ivana Trbojevic ◽  
Branka Ognjanovic ◽  
Natasa Djordjevic ◽  
Snezana Markovic ◽  
A.S. Stajn ◽  
...  

The role of oxidative stress in cisplatin (CP) toxicity and its prevention by pretreatment with selenium (Se) was investigated. Male Wistar albino rats were injected with a single dose of cisplatin (7.5 mg CP/kg b.m., i.p.) and selenium (6 mg Se/kg b.m, as Na2SeO3, i.p.) alone or in combination. The results suggest that CP intoxication induces oxidative stress and alters the glutathione redox status: reduced glutathione (GSH), oxidized glutathione (GSSG) and the GSH/GSSG ratio (GSH RI), resulting in increased lipid peroxidation (LPO) in rat liver. The pretreatment with selenium prior to CP treatment showed a protective effect against the toxic influence of CP on peroxidation of the membrane lipids and an altering of the glutathione redox status in the liver of rats. From our results we conclude that selenium functions as a potent antioxidant and suggest that it can control CP-induced hepatotoxicity in rats.


2020 ◽  
Vol 8 (1) ◽  
pp. 78
Author(s):  
Mohammed Kassem ◽  
Abdel-Fattah Ali ◽  
Seham Y. Abo-kora ◽  
Nesreen Shawky

This study investigates the modulating effect of ginseng against testicular toxicity, oxidative stress and changes in some biochemical parameters induced by doxorubicin. Twenty male rats were divided into four groups. The 1st group received distilled water orally (control group), The 2nd group received doxorubicin (5 mg/kg b.wt. intrapertenoineal) once a week for eight weeks, The 3rd group received ginseng extract (200 mg/kg b.wt.) daily for eight weeks and the 4th group received doxorubicin with ginseng extract by the same doses as in the 2nd and the 3rd groups respectively. At the end of the 8th week, blood and semen samples were taken for biochemical and semen analysis, respectively. The doxorubicin treated group had significantly higher serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), Creatine kinase (CK) and lactate dehydrogenase (LDH) along with lower levels of total protein, albumin and globulin. In addition, a significant decrease in antioxidant enzymes (SOD, CAT, GSHPx), and glutathione (GSH) associated with higher level of malondialdehyde (MDA) were observed. At the same time, the group that took doxorubicin with ginseng did not differ from control group in terms of these parameters. Male fertility study showed changes in testosterone and semen analysis in both groups treated with doxorubicin, while the group that took doxorubicin with ginseng showed an improvement towards control levels of these parameters. Thus ginseng supplement can reduce the negative effects of doxorubicin- induce.  


2021 ◽  
Vol 22 (15) ◽  
pp. 7765
Author(s):  
Youichirou Higashi ◽  
Takaaki Aratake ◽  
Takahiro Shimizu ◽  
Shogo Shimizu ◽  
Motoaki Saito

Stroke is a major cause of death worldwide, leading to serious disability. Post-ischemic injury, especially in the cerebral ischemia-prone hippocampus, is a serious problem, as it contributes to vascular dementia. Many studies have shown that in the hippocampus, ischemia/reperfusion induces neuronal death through oxidative stress and neuronal zinc (Zn2+) dyshomeostasis. Glutathione (GSH) plays an important role in protecting neurons against oxidative stress as a major intracellular antioxidant. In addition, the thiol group of GSH can function as a principal Zn2+ chelator for the maintenance of Zn2+ homeostasis in neurons. These lines of evidence suggest that neuronal GSH levels could be a key factor in post-stroke neuronal survival. In neurons, excitatory amino acid carrier 1 (EAAC1) is involved in the influx of cysteine, and intracellular cysteine is the rate-limiting substrate for the synthesis of GSH. Recently, several studies have indicated that cysteine uptake through EAAC1 suppresses ischemia-induced neuronal death via the promotion of hippocampal GSH synthesis in ischemic animal models. In this article, we aimed to review and describe the role of GSH in hippocampal neuroprotection after ischemia/reperfusion, focusing on EAAC1.


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