Investigation of protective effect of resveratrol and coenzyme Q10 against cyclophosphamide-induced lipid peroxidation, oxidative stress and DNA damage in rats.

It is seen that cyclophosphamide, which is used in treating many diseases, especially cancer, causes toxicity in studies, and its metabolites induce oxidative stress. This study aimed to investigate the protective effects of resveratrol and Coenzyme Q10, known for their antioxidant properties, separately and together, against oxidative stress induced by cyclophosphamide. In this study, 35 Wistar albino male rats were divided into five groups. Groups; Control group, cyclophosphamide (CP) group (CP as 75 mg kg i.p. on day 14), coenzyme Q10 (CoQ10) + CP group (20 mg/kg i.p. CoQ10 + 75 mg kg i.p. CP), resveratrol (Res) + CP group (20 mg/kg i.p. Res + 75 mg/kg i.p. CP), CoQ10 + Res + CP group (20 mg/kg i.p Res + 20 mg/kg i.p CoQ10 and 75 mg/kg i.p.CP). At the end of the experiment, the cholesterol, creatinine and urea levels of the group given CP increased, while a decrease was observed in the groups given Res and CoQ10. Malondialdehyde level was high, glutathione level, superoxide dismutase and catalase activities were decreased in the blood and all tissues (liver, kidney, brain, heart and testis) of the CP given group. DNA damage and histopathological changes were also observed. In contrast, Res and CoQ10, both separately and together, reversed the CP-induced altered level and enzyme activities and ameliorated DNA damage and histopathological changes. In this study, the effects of Res and CoQ10 against CP toxicity were examined both separately and together.

Investigation of the efficacy of epidermal growth factor, boric acid and their combination in cartilage injury in rats: An experimental study.

OBJECTIVES: In this study, we aimed to determine the bioefficacy of epidermal growth factor (EGF), boric acid (BA), and their combination on cartilage injury in rats. MATERIALS AND METHODS: In in vitro setting, the cytotoxic effects of BA, EGF, and their combinations using mouse fibroblast cell (L929), human bone osteosarcoma cell (Saos-2), and human adipose derived mesenchymal stem cells (hAD-MSCs) were determined by applying MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] test. In in vivo setting, 72 rats were randomly divided into four groups. A standard chondral defect was created and microfracture was performed in all groups. Group A was determined as the control group. In addition to the standard procedure, Group B received 100 ng/mL of EGF, Group C received a combination of 100 ng/mL of EGF and 10 µg/mL of BA combination, and Group D 20 µg/mL of BA. RESULTS: The cytotoxic effect of the combinations of EGF dilutions (1, 5, 10, 25, 50, 100, 200 ng/mL) with BA (100, 300, 500 µg/mL) was observed only in the 72-h application period and in Saos-2. The cytotoxic effect of BA was reduced when combined with EGF. There was no significant difference in the histopathological scores among the groups (p=0.13). CONCLUSION: Our study showed that EGF and low-dose BA application had a positive effect on cartilage healing in rats. Significant decreases in recovery scores were observed in the other groups. The combination of EGF and BA promoted osteoblast growth. Detection of lytic lesions in the group treated with 20 µg/mL of BA indicates that BA may have a cytotoxic effect.

Polydatin reduces aflatoxin-B1 induced oxidative stress, DNA damage, and inflammatory cytokine levels in mice.

This study showed the protective effect of polydatin (PD), which has an antioxidant activity against oxidative stress in mice caused by aflatoxin B1 (AFB1). In this study, 36 male Swiss albino mice were divided equally into 6 groups: 0.2 mL of FTS was administered to the control group, 0.2 mL of olive oil to the second group, and 0.75 mg/kg AFB1 to the third group by intragastric gavage every day for 28 days. The fourth, fifth, and sixth groups were administered 50, 100, and 200 mg/kg PD and 0.75 mg/kg AFB1 intragastrically for 28 days, respectively. AFB1 administration increased plasma aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, blood urea nitrogen, creatinine, and malondialdehyde levels in blood and tissue samples but decreased the level of glutathione and the activities of superoxide dismutase and catalase. On the other hand, it was determined that PD applications depending on the increasing doses brought these levels closer to normal. In addition, AFB1 administration increased the amount of ssDNA and liver COX-2, TNF-α, IL-6, NFκB, and Cyp3a11 mRNA expression levels; on the other hand, it decreased the IL-2 mRNA expression level. In contrast, increasing doses of PD application regulated the amount of ssDNA and these mRNA expression levels. Additionally, histopathological damage was observed in the liver and kidney tissues of the AFB1 group, while PD applications in a dose-dependent manner improved these damages. As a result, it was determined that PD reduced AFB1-induced oxidative stress, DNA damage, and inflammation and exhibited a protective effect on tissues in mice.

Acetaminophen-Induced Nephrotoxicity: Suppression of Apoptosis and Endoplasmic Reticulum Stress Using Boric Acid.

Acetaminophen (APAP) is one of the popular and safe pain medications worldwide. However, due its wide availability, it is frequently implicated in intentional or unintentional overdoses where it can cause severe liver injury and even acute liver failure. Boron is a bioactive trace element, found naturally as boric acid (BA) and borate. In this study, the effects of boric acid on the acute renal toxicity induced by APAP in rats were researched in comparison with N-acetyl cysteine (NAC). In the study, 7 groups were formed and 2 g/kg dose of paracetamol per rat was prepared by suspending in 1% Carboxy Methyl Cellulose (CMC) solution of phosphate buffer saline (PBS). Boric acid dissolved in saline was administered to experimental animals by gavage at doses of 50, 100, and 200 mg/kg. In this study, ER stress and apoptosis formed by paracetamol-induced nephrotoxicity were investigated. This purpose determined iNOS, PERK, ATF6, NFkB p53, caspases 3, 12, bcl-2, and bcl-xL gene mRNA expression kidney tissue. Also, the levels of kidney injury molecule-1 (KIM-1), Cysteine (Cys), and IL-18 levels, which are mentioned today as kidney damage markers were compared with BUN and creatine levels. The effect of boron on kidney damage was determined by histopathologic. Data were statistically analyzed by using SPSS-20 ANOVA and stated as means and standard deviation. According to the data obtained in our study, we believe that boric acid has a protective effect on the negative effects of paracetamol on the kidney. We believe that our study will provide useful data to the literature on the possibility of a supplement to be used as an active compound in paracetamol for the prophylaxis of boric acid and it can also be converted into a useful product.

The effects of boron-supplemented diets on adipogenesis-related gene expressions, anti-inflammatory, and antioxidative response in high-fat fed rats.

The fatty liver syndrome caused by nutritional factors is a common cause of hepatic dysfunction globally. This research was designed to study the shielding effect of boron in rats fed a diet having high fat. Overall, 40 Wistar albino male rats were placed into one control and four treatment groups, that is, each having eight rats. Group I was provided with a standard rat diet while group II was only provided a high-fat diet for 60 days. Groups III, IV, and V were provided with 5, 10, and 20 mg/kg/day boron, respectively, by gastric gavage besides a high-fat diet for 60 days. Malondialdehyde was increased significantly in rats' blood and tissue because of high-fat diets. Glutathione was decreased significantly in blood and tissues because of a high-fat diet. Moreover, the activities of superoxide dismutase (SOD) and catalase (CAT) were decreased in the blood and tissues of the high-fat-fed rats. The genes expression for C-reactive protein, interleukin-1ß, leptin, and tumor necrosis factor-α were increased while gene expression for peroxisome proliferator-activated receptors was decreased in the liver of rats fed with a high-fat diet. Contrariwise, boron supplementation improves antioxidative response in terms of increased SOD and CAT activities, gene expression regulation, and improved anti-inflammatory activities. In a nutshell, boron has dose-dependent shielding antioxidative and tissue regenerative effects in rats.

Resveratrol alleviates pyraclostrobin-induced lipid peroxidation, oxidative stress, and DNA damage in rats.

Pyraclostrobin (Pyra) is a fungicide in the strobilurin class and has proven to be very toxic to organisms primarily aquatic species. Resveratrol (Res) is a phytoalexin that exhibits multiple bioactivities as anti-oxidative, anti-inflammatory, cardiovascular protective, and anti-aging and is found in plant species such as mulberry, peanut, and grape. This study aimed to determine the protective effect of Res against Pyra-induced lipid peroxidation, oxidative stress, and DNA damage in rats. For this purpose, a total of 48 male rats divided into 6 groups - 8 in each group - were exposed to 30 mg/kg Pyra by oral gavage once a day for 30 days and to three different concentrations of Res (5, 10, and 20 mg/kg) together with Pyra. Pyra administration increased liver enzyme parameters and malondialdehyde (MDA) levels whereas decreased glutathione (GSH) levels and activities of superoxide dismutase (SOD) and catalase (CAT). Also, Pyra treatment increased pro-apoptotic (Bax), apoptotic (Caspase-3, Caspase-8, and Caspase-9), pro-inflammatory (NFκB), cancer (CYP2E1), and cell regulatory (p53) gene expressions and decreased anti-apoptotic (Bcl-2) gene expression in the liver. Furthermore, DNA damage in blood and histopathological changes in the liver and kidney were observed with Pyra administration. In contrast, Res administrations in a dose-dependent manner improved Pyra-induced lipid peroxidation, oxidative and DNA damages, expression levels of these genes in the liver, and histopathological changes in the liver and kidney. Consequently, the treatment of Res, known for its anti-oxidant and protective properties, exhibited a protective effect on Pyra-induced lipid peroxidation, oxidant/anti-oxidant status, gene expressions, and DNA damage in rats.

Natural Products/Bioactive Compounds as a Source of Anticancer Drugs.

Cancer is one of the major deadly diseases globally. The alarming rise in the mortality rate due to this disease attracks attention towards discovering potent anticancer agents to overcome its mortality rate. The discovery of novel and effective anticancer agents from natural sources has been the main point of interest in pharmaceutical research because of attractive natural therapeutic agents with an immense chemical diversity in species of animals, plants, and microorganisms. More than 60% of contemporary anticancer drugs, in one form or another, have originated from natural sources. Plants and microbial species are chosen based on their composition, ecology, phytochemical, and ethnopharmacological properties. Plants and their derivatives have played a significant role in producing effective anticancer agents. Some plant derivatives include vincristine, vinblastine, irinotecan, topotecan, etoposide, podophyllotoxin, and paclitaxel. Based on their particular activity, a number of other plant-derived bioactive compounds are in the clinical development phase against cancer, such as gimatecan, elomotecan, etc. Additionally, the conjugation of natural compounds with anti-cancerous drugs, or some polymeric carriers particularly targeted to epitopes on the site of interest to tumors, can generate effective targeted treatment therapies. Cognizance from such pharmaceutical research studies would yield alternative drug development strategies through natural sources which could be economical, more reliable, and safe to use.

Antioxidant and cytoprotective effects of N-acetylcysteine against subchronic oral glyphosate-based herbicide-induced oxidative stress in rats.

It is claimed that oxidative stress has a prominent role in the mechanism of toxic effects formed by glyphosate-based herbicide (GBH) in living systems. A strong thiol compound, N-acetylcysteine (NAC), has antioxidative and cytoprotective properties. The objective in this subchronic toxicity study was to identify the prophylactic effect of NAC over histopathological changes and oxidative stress induced by GBH in blood, renal, liver, cardiac, and brain tissues. A sum of 28 male Wistar rats were divided into four equal groups, each containing 7 rats. During the study, group I (control group) was supplied with normal rodent bait and tap water ad libitum. The applied agents were 160 mg/kg NAC to group II, 375 mg/kg as equivalent to 1/10 of lethal dose 50% (LD50) of GBH to group III, and 160 mg/kg of NAC and 375 mg/kg of GBH together once per day as oral gavage to group IV for 8 weeks. While GBH decreased the levels of GSH in blood, liver, kidney, and brain tissues, it considerably increased malondialdehyde levels. On the contrary, these parameters happened to improve in the group supplied with NAC. Besides, it was seen that NAC was observed to improve the histopathologic changes in rat tissues induced by GBH. It was concluded that NAC protects oxidative stress and tissue damage induced by GBH in blood and tissue and this prophylactic effect could be attributed to its antioxidant and free radical sweeper character.

The ameliorative effects of boron against acrylamide-induced oxidative stress, inflammatory response, and metabolic changes in rats.

Acrylamide (ACR) is a hazardous substance associated with the accumulation of excessive reactive oxygen species and causes oxidative stress. Presence of ACR in foods leads to public health concerns due to its known neurotoxic, genotoxic, and carcinogenic effects. The present study investigated the ameliorative effects of boron (B) against ACR exposed rats. Forty Wistar albino male rats, fed with low-boron diet, were randomly and equally allocated into 5 groups. The control group was orally treated with physiological saline as placebo, the second group was orally given 15 mg/kg ACR. The other groups were orally treated with 15 mg/kg ACR and B at the levels of 5, 10, and 20 mg/kg/day for 60 days, respectively. ACR-treatment significantly increased malondialdehyde levels whereas decreased glutathione levels in rat tissues. Also, ACR-treatment increased the activities of superoxide dismutase and catalase in erythrocytes and tissues. Meanwhile, mRNA expression levels of NFĸB, IFN-γ, IL-1ß, and TNF-α in liver and brain of rats were increased under ACR treatment. Additionally, ACR caused a significant decrease in the level of high-density lipoprotein, with increase in the levels of low-density lipoprotein, triglyceride, cholesterol, glucose, urea nitrogen, and creatinine. Lastly, B alleviated histopathological alterations induced by ACR in rat tissues.

In vivo assessment of polydatin, a natural polyphenol compound, on arsenic-induced free radical overproduction, gene expression, and genotoxicity.

Arsenic (As) is a well-known contaminant of global groundwater. Its exposure causes several hazardous effects on animals and human via oxidative stress. The present study examined the effect of polydatin (PD) on free radical overproduction in rats exposed to As. Thirty-five male rats randomly allocated into five equal groups. To the control group, physiological saline was given orally and to the second group only 100 mg/L As was given by drinking water for 60 days. The other groups were treated with As (100 mg/L) and PD orally at 50, 100, and 200 mg/kg/day, respectively. Treatment with As enhanced malondialdehyde level but decreased glutathione level in blood, liver, kidney, brain, lung, and heart of rats. Also, As decreased superoxide dismutase and catalase activities of erythrocyte, liver, kidney, brain, lung, and heart in rats. Furthermore, As treatment gave rise to increased DNA damage and gene expressions of interleukin 1 beta (IL-1ß), nuclear factor kappa beta (NFκB), p53, and tumor necrosis factor-α (TNF-α) in the lung, brain, kidney, and liver. However, treatment of PD ameliorated As-exposed lipid peroxidation, antioxidant enzymes activities, DNA damage, gene expressions, and histopathological changes in tissues. In conclusion, PD has a dose-dependent protective effect on lipid peroxidation and antioxidant defense mechanism in rats against As exposure.

Determination of the regulatory properties of Yucca schidigera extracts on the biochemical parameters and plasma hormone levels associated with obesity

ABSTRACT Yucca schidigera Ortgies, Asparagaceae, is a herbaceous plant. Due to the high saponin content the powdered branches and leaves are used as natural food additive for human and animal. The aim of this study was to investigate the effects of Y. schidigera extracts on plasma leptin, ghrelin, adiponectin, insulin, thyroid hormones and some biochemical parameters in mice fed a high-fat diet. Male Swiss Albino mice were divided into seven equal groups. Group I (negative control group) was given standard diet; Group II was given high-fat diet; Group III was given high-fat diet with carboxymethylcellulose; Groups IV–VII were given hexane, petroleum ether, ethyl acetate, and methanol extracts of Y. schidigera and high-fat diet via gastric gavage for 60 days. High-fat diet significantly increased plasma leptin, insulin, free T3 hormone, glucose, cholesterol, low-density lipoprotein, triacylglyceride, aspartate aminotransferase and alanine aminotransferase levels, and significantly decreased plasma ghrelin, adiponectin and free T4 hormone levels. On the other hand, hormone levels, lipid profile and biochemical parameters were improved by the administration of the PE extract. Y. schidigera extracts could be used as preventive medicine in nutritional disorders via regulating energy metabolism and hormonal functions.

The Effects of Boron on Arsenic-Induced Lipid Peroxidation and Antioxidant Status in Male and Female Rats.

The aim of the present study was to investigate the possible protective effects of boron, an antioxidant agent, against arsenic-induced oxidative stress in male and female rats. In total, 42 Wistar albino male and female rats were divided into three equal groups: The animals in the control group were given normal drinking water, the second group was given drinking water with 100 mg/L arsenic, and the third group was orally administered drinking water with 100 mg/kg boron together with arsenic. At the end of the 28-day experiment, arsenic increased lipid peroxidation and damage in the tissues of rats. However, boron treatment reversed this arsenic-induced lipid peroxidation and activities of antioxidant enzymes in rats. Moreover, boron exhibited a protective action against arsenic-induced histopathological changes in the tissues of rats. In conclusion, boron was found to be effective in protecting rats against arsenic-induced lipid peroxidation by enhancing antioxidant defense mechanisms.

Boron attenuates malathion-induced oxidative stress and acetylcholinesterase inhibition in rats.

Organophosphorus compounds cause oxidative stress and lead to alterations in antioxidant status in organisms. In this study, the effects of subchronic exposure to malathion and the protective effects of boron (B) were evaluated in 48 Wistar rats, which were divided equally into six groups. For 28 d, the control group received a normal diet and tap water, the corn oil group received a normal diet and 0.5 mL of corn oil by gastric gavage and the malathion group received a normal diet and malathion (100 mg/kg/d) by gastric gavage. During the same period, each of the three other groups received a different dosage of B (5, 10 and 20 mg/kg/d, respectively) and malathion (100 mg/kg/d) by gastric gavage. Malathion administration during the period increased malondialdehyde, nitric oxide and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels, as well as markers of liver function, yet decreased acetylcholinesterase, reduced glutathione, superoxide dismutase, and catalase activities in blood, liver, kidney and brain tissues. Administration of B in a dose-dependent manner also reversed malathion-induced oxidative stress, lipid peroxidation (LPO) and antioxidant enzyme activity. Moreover, B exhibited protective action against malathion-induced histopathological changes in liver, kidney and brain tissues. These results demonstrate that, if used in a dose-dependent manner, B decreases malathion-induced oxidative stress, enhances the antioxidant defense mechanism and regenerates tissues in rats.

Protective effect of polydatin, a natural precursor of resveratrol, against cisplatin-induced toxicity in rats.

The aim of the present study was to evaluate the possible protective effect of polydatin (PD) on cisplatin (Cis) induced oxidative stress in rats. Totally, thirty male Wistar albino rats were fed standard rodent diet and divided into 5 equal groups: the control group (vehicle treated) was treated with physiological saline for ten days both orally and intraperitoneally (i.p.), the second group was orally treated with physiological saline and 7 mg/kg single i.p. injection of Cis on the seventh day, and third, fourth, and fifth groups were treated orally PD at 25, 50, and 100 mg/kg/day, respectively for 10 days starting seven days before Cis injection and 7 mg/kg single i.p. Cis was injected on the seventh day. Cis resulted in significant increase malondialdehyde levels and decreased glutathione levels. In addition, Cis treatment decreased superoxide dismutase and catalase activities in erythrocyte and tissues. Also, Cis treatment caused to increase DNA damage and affected serum biochemical parameters whereas slightly decreased AchE activity. However, treatment of PD resulted in reversal of Cis-induced oxidative stress, lipid peroxidation, and activities of antioxidant enzymes. In conclusion, PD has protective effect in rats against Cis-induced oxidative stress, enhances antioxidant defence mechanism, and regenerates their tissues.

Protective effects of boron on cyclophosphamide induced lipid peroxidation and genotoxicity in rats.

The aim of the present study was to evaluate the possible protective effect of boron (B) on cyclophosphamide (CYC) induced oxidative stress in rats. Totally, thirty Wistar albino male rats were fed standard rodent diet and divided into 5 equal groups: physiological saline was given intraperitoneally (i.p.) to the control group (vehicle treated), to the second group only 75 mg kg(-1) CYC was given i.p. on the 14th d, and boron was administered (5, 10, and 20 mg kg(-1), i.p.) to the other groups for 14 d and CYC (75 mg kg(-1), i.p.) on the 14th d. CYC caused increase of malondialdehyde and decrease of glutathione levels, decrease of superoxide dismutase activities in erythrocyte and tissues, decrease of erythrocyte, heart, lung, and brain catalase, and plasma antioxidant activities. Also, CYC treatment caused to DNA damage in mononuclear leukocytes. Moreover, B exhibited protective action against the CYC-induced histopathological changes in tissues. However, treatment of B decreased severity of CYC-induced lipid peroxidation and genotoxicity on tissues. In conclusion, B has ameliorative effects against CYC-induced lipid peroxidation and genotoxicity by enhancing antioxidant defence mechanism in rat.

Dietary Yucca schidigera supplementation reduces arsenic-induced oxidative stress in Swiss albino mice.

The aim of this study was to clarify the effects of dietary supplementation with Yucca schidigera (Ys) on lipid peroxidation (LPO), antioxidant activity, some biochemical parameters and histopathological changes in arsenic-exposed mice. Forty Swiss albino male mice were divided into five equal groups. Group I (control group) was given normal diet and tap water for 28 days. Group II (arsenic group) was given normal diet and 100 mg/L arsenic along with drinking water for 28 days. Groups III-V were given three different doses of Ys (50, 100 and 200 mg/kg) in supplemented diet and arsenic (100 mg/L) along with drinking water throughout the entire period of 28 days. The arsenic significantly increased serum biochemical parameters and malondialdehyde levels in blood and tissue. However, arsenic significantly decreased tissue glutathione concentration, erythrocyte superoxide dismutase and catalase activities. In contrast, dietary supplementation of Ys, in a dose-dependent manner, resulted in reversal of arsenic-induced oxidative stress, LPO and activities of antioxidant enzymes. Moreover, Ys also exhibited protective action against the arsenic-induced focal gliosis and hyperemi in brain, necrosis and degeneration in liver, degeneration and dilatation in Bowman's capsule of kidney and hyaline degeneration in heart tissue of mice. Consequently, our results demonstrate that Ys especially high-dose supplementation in diet decreases arsenic-induced oxidative stress and enhances the antioxidant defence mechanism and regenerate of tissues in Swiss albino mice.

Protective effect of boric acid against carbon tetrachloride-induced hepatotoxicity in mice.

The protective effect of boric acid against liver damage was evaluated by its attenuation of carbon tetrachloride (CCl(4))-induced hepatotoxicity in mice. Male albino mice were treated intraperitoneally (i.p.) with boric acid (50, 100, and 200 mg/kg) or silymarin daily for 7 days and received 0.2% CCl(4) in olive oil (10 mL/kg, i.p.) on day 7. Results showed that administration of boric acid significantly reduced the elevation in serum levels of aspartate aminotransferase, alkaline phosphatase, alanine aminotransferase, and the level of malondialdehyde in the liver that were induced by CCl(4) in mice. Boric acid treatment significantly increased glutathione content, as well as the activities of superoxide dismutase and catalase in the liver. Boric acid treatment improved the catalytic activity of cytochrome P450 2E1 and maintained activation of nuclear factor kappa light-chain enhancer of activated B cell gene expression, with no effect on inducible nitric oxide synthase gene expression in the livers of mice. Histopathologically, clear decreases in the severity of CCl(4)-induced lesions were observed, particularly at high boric acid concentrations. Results suggest that boric acid exhibits potent hepatoprotective effects on CCl(4)-induced liver damage in mice, likely the result of both the increase in antioxidant-defense system activity and the inhibition of lipid peroxidation.

The effects of Feijoa sellowiana fruits on the antioxidant defense system, lipid peroxidation, and tissue morphology in rats.

CONTEXT: The fruits of Feijoa sellowiana Berg. (Myrtaceae) have been used to treat goiter in traditional Turkish medicine. OBJECTIVE: To evaluate the in vivo antioxidant activities of different polarities of the fruit extracts in blood and tissue (liver, kidney, brain, and heart) antioxidant defense systems in standard pellet diet and in high fat diet consumed, male rats were assessed. MATERIALS AND METHODS: The extracts (methanol, n-hexane, chloroform, ethyl acetate, n-butanol, and aqueous) were administered orally to male rats at 50 mg/kg doses daily for 4 weeks. The blood and tissue malondialdehyde (MDA), reduced glutathione (GSH) levels, plasma nitrate (NO(x)) level, total triiodothyronine (T3), thyroxine, cholesterol, triglyceride, protein, and glucose levels were determined, and erythrocyte superoxide dismutase (SOD) and catalase (CAT) activities; plasma antioxidant activity (AOA) were experimentally studied. RESULTS: Blood MDA level (7.81 ± 0.4) was significantly decreased; GSH level (29.65 ± 1.21) and AOA (1.52 ± 0.08) were increased in ethyl acetate extract as compared with control and the other extracts. In addition, all the extracts decreased MDA levels and increased GSH levels (except brain tissue homogenate) in the tissue homogenates. Erythrocyte SOD and CAT activity levels were unchanged in F. sellowiana extracts. However, the extracts had no effect on plasma NO(x). In the histopathological examinations, any changes or damage in the vital organs were seen in animals. CONCLUSION: The experimental data demonstrated that F. sellowiana extracts displayed remarkable antioxidant activity and decreased lipid peroxidation in rats; furthermore, no histopathological changes or damage have been observed in the vital organs of rats.

Prophylactic effect of N-acetylcysteine against sodium fluoride-induced blood oxidative stress in mice.

Ninety female Balb/c mice were used. The animals were allocated to evenly six groups. While the first group was maintained as control, Groups 3, 4, 5, and 6 were administered 750 ppm, 1500 ppm, 3000 ppm, and 6000 ppm of N-acetylcysteine, respectively, for a period of 15 days. After day 15, Groups 2-6 were administered sodium fluoride, containing 100 ppm fluoride in drinking water, for another 15 days. Plasma malondialdehyde (MDA) levels and erythrocyte superoksid dismutase (SOD) and catalase (CAT) activities were determined at the beginning of the trial and on days 15 and 30. According to the data obtained in the present study, N-acetylcysteine, when administered at the indicated doses, did not produce a significant alteration in any of the three parameters investigated. On the other hand, while the plasma MDA level was determined to have increased significantly, erythrocyte SOD and CAT activities were ascertained to have decreased significantly in the group, which was administered sodium fluoride alone on day 30. In the groups, which were administered N-acetylcysteine prior to sodium fluoride, however, it was observed that, after sodium fluoride administration, plasma MDA levels and erythrocyte SOD and CAT activities drew closer to the values of the control group.

The effects of dietary boric acid and borax supplementation on lipid peroxidation, antioxidant activity, and DNA damage in rats.

The aims of this study were to clarify the effects of high dietary supplementation with boric acid and borax, called boron (B) compounds, on lipid peroxidation (LPO), antioxidant activity, some vitamin levels, and DNA damage in rats. Thirty Sprague Dawley male rats were divided into three equal groups: the animals in the first group (control) were fed with a standard rodent diet containing 6.4 mg B/kg, and the animals in the experimental group were fed with a standard rodent diet added with a supra-nutritional amount of boric acid and borax (100 mg B/kg) throughout the experimental period of 28 days. The B compounds decreased malondialdehyde (MDA), DNA damage, the protein carbonyl content (PCO) level in blood, and glutathione (GSH) concentration in the liver, Cu-Zn superoxide dismutase (SOD), and catalase (CAT) activity in the kidney. The B compounds increased GSH concentration in blood and the vitamin C level in plasma. Consequently, our results demonstrate that B supplementation (100 mg/kg) in diet decreases LPO, and enhances the antioxidant defense mechanism and vitamin status. There are no differences in oxidant/antioxidant balance and biochemical parameters except for serum vitamin A and liver GSH concentration, between the boron compounds used in this study.