Palm oil extracts protected against cadmium chloride poisoning via inhibition of oxidative stress in rats

Background The probable mechanism of an earlier reported capacity of palm oil extracts to confer protection against high dose cadmium poisoning in rats was reported in this study. Similar experimental design earlier reported by us was retained. Rats therefore were sacrificed at intervals of twelve; twenty four and forty eight hours post CdCl2 insult. Results Oxidative stress and antioxidant status (malondialdehyde, superoxide dismutase, catalase and glutathione) were assessed in tissues (liver, kidney, heart, brain, muscle) and serum. Oxidative stress indicators showed a significantly (p < 0.05) increased lipid peroxidation and alterations in antioxidant defence systems occasioned by drop in catalase and superoxide dismutase enzymes (serum, liver, heart, brain and kidneys) of the rats. Also observed were significant (p < 0.05) reduction in the non-enzymatic antioxidant reduced glutathione over time. Pre-administration of rats with the crude palm oil and its extracts modulated cadmium mediated depletion of the antioxidant capacities of rats acutely exposed to cadmium and rising lipid peroxidation profile. Conclusions Regulation of stress and antioxidant response was the underlying mechanism by which the extracts conferred protection against high dose cadmium insult thus suggesting its potential as a viable therapeutic target against its deleterious effects. Graphical Abstract

Palm oil extracts’ protected against cadmium chloride poisoning via inhibition of oxidative stress in rats”

Background: The probable mechanism of an earlier reported capacity of palm oil extracts to confer protection against high dose cadmium poisoning in rats was reported in this study. Similar experimental design earlier reported by us was retained. Rats therefore were sacrificed at intervals of twelve; twenty four and forty eight hours post CdCl2 insult. Results: Oxidative stress and antioxidant status (malondialdehyde, superoxide dismutase, catalase and glutathione) were assessed in tissues (liver, kidney, heart, brain, muscle) and serum. Oxidative stress indicators showed a significantly (p<0.05) increased lipid peroxidation and alterations in antioxidant defence systems occasioned by drop in catalase and superoxide dismutase enzymes (serum, liver, heart, brain and kidneys) of the rats. Also observed were significant (p<0.05) reduction in the non-enzymatic antioxidant reduced glutathione over time. Pre-administration of rats with the crude palm oil and its extracts modulated cadmium mediated depletion of the antioxidant capacities of rats acutely exposed to cadmium and rising lipid peroxidation profile. Conclusions: Regulation of stress and antioxidant response was the underlying mechanism by which the extracts conferred protection against high dose cadmium insult thus suggesting its potential as a viable therapeutic target against its deleterious effects.

Ureides are similarly accumulated in response to UV-C irradiation and wound but differently remobilized during recovery in Arabidopsis leaves

To examine a role of purine degraded metabolites in response to wounding or UV-C stress, the Arabidopsis wild-type (WT) and Atxdh1 KO mutants, defective in xanthine dehydrogenase1 (XDH1), were exposed to wounding and UV-C irradiation stress. In Atxdh1 mutant, wounding or UV-C stresses resulted in lower fresh-weight, increased senescence symptoms and higher tissue cell death rate compared to WT plants. Additionally, WT plants exhibited lower levels of oxidative stress indicators; reactive oxygen species and malondialdehyde than Atxdh1 mutant leaves. Notably, Transcripts and Proteins functioning in purine degradation pathway were orchestrated to lead to enhanced ureide levels in WT leaves 24 h after applying UV-C or wound stress. Yet, different remobilization of the accumulated ureides was noticed 72 h after stresses application. In plants treated with UV-C the allantoin level was highest in young leaves, whereas in wounded plants it was lowest in the young leaves, accumulated mainly in the middle and wounded leaves. The results indicate that in UV-C treated WT plants, during the recovery period from stress, ureides are remobilized from the lower older leaves to support young leaf growth. In contrast, after wounding, the ureides are remobilized to the young leaves, yet more to the middle wounded leaves, to function as antioxidants and/or healing agents.

Analysis of oxidative stress indicators in Polish patients with prostate cancer

The aim of the study was to analyze the activity of antioxidant enzymes (glutathione S-transferase, catalase, superoxide dismutase) and the concentration of malondialdehyde in order to determine the role of detoxification mechanisms in prostate cancer. The activities of superoxide dismutase (SOD), catalase (CAT), and glutathione S-transferase (GST) were measured using ready-made kits; lipid peroxidation intensity was determined by the thiobarbituric acid method. Superoxide dismutase was the only enzyme among antioxidant and detoxification enzymes for which a statistically significant difference in activity was found between the studied groups (1.4 U·ml−1 in patients vs. 1.6 U·ml−1 in control). No statistically significant differences were found for GST, CAT or the concentration of MDA between the group of men with prostate cancer and the control group. The lower SOD activity in men with prostate cancer may be due to a deficiency in their antioxidant defense system.

GC-MS-Based Serum Metabolomic Investigations on the Ameliorative Effects of Polysaccharide from Turpiniae folium in Hyperlipidemia Rats

Hyperlipidemia, a typical metabolic disorder syndrome, can cause various cardiovascular diseases. The polysaccharides were found to have enormous potential in the therapy of hyperlipidemia. This study was aimed at evaluating the ameliorative effects of polysaccharide from Turpiniae folium (TFP) in rats with hyperlipidemia. A serum metabolomic method based on gas chromatography-mass spectrometry (GC-MS) was used to explore the detailed mechanism of TFP in rats with hyperlipidemia. The oxidative stress indicators, biochemical indexes, and inflammatory factors in serum and histopathological changes in the liver were also evaluated after 10-week oral administration of TFP in rats with high-fat diet-induced hyperlipidemia. TFP significantly relieved oxidative stress, inflammation, and liver histopathology and reduced blood lipid levels. Multivariate statistical approaches such as principal component analysis and orthogonal projection to latent structure square-discriminant analysis revealed clear separations of metabolic profiles among the control, HFD, and HFD+TFP groups, indicating a moderating effect of TFP on the metabolic disorders in rats with hyperlipidemia. Seven metabolites in serum, involved in glycine, serine, and threonine metabolism and aminoacyl-tRNA biosynthesis, were selected as potential biomarkers in rats with hyperlipidemia and regulated by TFP administration. It was concluded that TFP had remarkable potential for treating hyperlipidemia. These findings provided evidence for further understanding of the mechanism of action of TFP on hyperlipidemia.

NEUROPROTECTIVE EFFECT OF WATERMELON (CITRULLUS LANATUS) PULP JUICE ON SCOPOLAMINE-INDUCED MEMORY DEFICITS IN SWISS ALBINO MICE: THE ROLE OF ACETYLCHOLINESTERASE AND OXIDATIVE STRESS

The effect of Watermelon (Citrullus lanatus) Pulp Juice (WPJ) on scopolamine (SCOP) induced memory deficits is due to the involvement of oxidative stress and AChE activity. The juice was obtained by crushing the pulp in blender and three different concentrations of 100%, 50% and 25% was administration to prevent memory deficit by evaluating changes of AChE activity and oxidative stress indicators (SOD, CAT, LPO and GPx) induced by scopolamine. These results provide evidence that WPJ is an alternative to protect SCOP induced memory deficits in mice by involvement of oxidative stress and AChE activity.

Ureides are similarly accumulated in response to UV-C irradiation and wound but differently remobilized during recovery in Arabidopsis leaves.

To examine a role of purine degraded metabolites in response to wounding or UV-C stress, the Arabidopsis wild-type and Atxdh1 KO mutants, defective in xanthine dehydrogenase1 (XDH1), were exposed to wounding and UV-C irradiation stress. In Atxdh1 mutant, wounding or UV-C stresses resulted in lower fresh-weight, increased senescence symptoms and higher tissue cell death rate compared to Wild-type. Additionally, Wild-type exhibited lower levels of oxidative stress indicators; reactive oxygen species and malondialdehyde than Atxdh1 mutant leaves. Notably, purine degradation transcripts and proteins were orchestrated to lead to enhanced ureide levels in Wild-type leaves 24 h after applying UV-C or wound stress. Yet, different remobilization of the accumulated ureides was noticed 72 h after stresses application. In plants treated with UV-C the allantoin level was highest in young leaves, whereas in wounded plants it was lowest in the young leaves, accumulated mainly in the middle and wounded leaves. The results indicate that in UV-C treated Wild-type, during the recovery period from stress, ureides are remobilized from the lower older leaves to support young leaf growth. In contrast, after wounding, the ureides are remobilized to the young leaves, yet more to the middle wounded leaves, to function as antioxidants and/or healing agents.

The effects of carvacrol on oxidative stress, inflammation, and liver function indicators in a systemic inflammation model induced by lipopolysaccharide in rats

The effect of carvacrol (CAR) on oxidative stress, inflammation, and liver dysfunction induced by lipopolysaccharide (LPS) was explored. The rats (n=40) were daily injected (2 weeks) by saline as control, LPS (1 mg/kg, i.p.), and 25, 50 or 100 mg/kg CAR (i.p.) before LPS. LPS increased aspartate transaminase (AST: 162±13 U/L), alanine aminotransferase (ALT: 74.6±2.15 U/L), alkaline phosphatase (ALK-P: 811±51 U/L), interlukine-1β (IL-1β: 1254±51 pg/g tissue), malondialdehyde (MDA: 32±1.09 nM/g tissue), and nitric oxide (NO: 224±13.5 nM/g tissue) (P<0.01–P<0.001) while, decreased total protein(4.08±0.38 g/dl), albumin(2.79±0.16 g/dl), thiol (5.16±0.19 μM/g tissue), superoxide dismutase (SOD: 10.57±0.13 U/g tissue), and catalase (CAT: 0.78±0.02 U/g tissue) compared to control (P<0.001). CAR reversed the effects of LPS (P<0.05–P<0.001). In the rats treated by 100 mg/kg CAR, the indicators were as follows: AST: 118±10.1 U/L, ALT: 42.5±4.13 U/L, ALK-P: 597±39.91 U/L, IL-1β: 494±15 pg/g tissue, and NO: 141±5.35 nM/g tissue. Both 50 and 100 mg/kg CAR corrected oxidative stress indicators and in the group treated by 100 mg/kg CAR, they were: MDA: 23.4±0.91 nM/g tissue, thiol: 7.98±0.18 μM/g tissue, SOD: 21±0.8 U/g tissue, and CAT: 1.12±0.02 U/g tissue(P<0.05–P<0.001). In conclusion, CAR improved liver function, accompanied with antioxidant and antiinflammatory effects.