The Vitamin D Binding Protein Gene Polymorphism Association with Covid-19-Infected Iraqi Patients.

Vitamin D deficiency, in general, is usually correlated with increased risks of chronic pulmonary disease such as COVID-19 infection. However, the mechanisms are still unknown. Herein, this study aimed to investigate the correlation between vitamin D binding protein gene polymorphism and COVID-19-infected Iraqi patients. The study has been conducted on patients with Covid-19 during the period extended from June, 2021 to April, 2022. 300 samples were collected from healthy and infected people. The demographic characteristics of patients (age, gender and residency) are shown non-significant in all. However, the distribution of DBP (rs12785878-T/G) Polymorphism was detected by Allele Specific PCR technique. The association between DBP (rs12785878) gene polymorphism and risk of Covid-19 is also shown, the heterozygous genotype TG was more frequent in the patients' group in comparison with the control group, 66 versus 58, respectively. Therefore, genotype TG was a genetic risk factor for Covid-19 with an odds ratio of 2.4074 (95% confidence interval of 1.2462-4.6505) and an etiologic fraction of 0.2963. In the addition, the homozygous genotype GG was more frequent in the patients' group in comparison with the control group, 65 versus 54, respectively, Therefore, genotype GG was a risk factor for Covid-19 with an odds ratio of 1.0578 (95% confidence interval of 0.6386-1.7522) and an etiologic fraction of 0.0299. thus, it can be seen that Covid-19 disease has a direct effect on the level of vitamin D in patients infected with the virus compared to healthy people.

The rs1801280 SNP is associated with non-small cell lung carcinoma by exhibiting a highly deleterious effect on N-acetyltransferase 2.

PURPOSE: N-acetyltransferase 2 is an enzyme that is involved in the detoxification of carcinogens in the human body, so any damage to this protein may lead to the emergence of several metabolic dysfunctions. This work was conducted to determine the association between NAT2 polymorphism and non-small cell lung carcinoma (NSCLC) that is increasingly reported in the Iraqi population. METHODS: PCR sequencing was conducted to assess the possible association between genetic variants and NSCLC. Several in silico tools were implemented to investigate the effect of the observed SNPs on the structure, function, and stability of the altered NAT2. RESULTS: Five SNPS of NAT2 (rs1208, rs1041983, rs1799929, rs1799930, and rs1801280) were identified in high frequencies in the amplified fragment. These SNPs showed variable distributions of haplotypes between cases and controls. No significant association of rs1208, rs1041983, rs1799929, and rs1799930 with NSCLC was shown in the investigated population. In contrast, rs1801280: CC genotype showed a highly significant (P = 0.009) association with the NSCLC, and individuals with this genotype had 2.19 more chances for developing NSCLC (OR 2.19; Cl95% 1.21-3.94). Association analysis of rs1801280 SNP distribution among the investigated patients showed that patients with CC genotype showed a significant (P = 0.02, OR 2.65) association with family history, which entailed a high hereditary possibility of this genotype among Iraqi patients. It was predicted that this SNP showed high damaging effects on the activity of NAT2 enzyme, with various deleterious outcomes on enzyme structure, function, and stability. CONCLUSION: Data indicated that rs1801280 SNP exerted a tight association with NSCLC since individuals with CC genotype exhibited the most damaging effects on the NAT2 that may be behind the low acetylation rates of this enzyme in patients with NSCLC.

Two missense variants of the epidermal growth factor receptor gene are associated with non small cell lung carcinoma in the subjects from Iraq.

BACKGROUND: Lung carcinoma is a foremost cause of cancer-related mortality worldwide. Variable genetic factors are associated with the development of lung cancer. This study was performed to evaluate the possible association of epidermal growth factor receptor (EGFR) gene polymorphisms with non small cell lung carcinoma (NSCLC) in Iraqi population. METHODS: DNA samples were extracted from 100 patients and 100 controls. Four PCR fragments were designed to amplify four high-frequency variants within EGFR, namely rs1050171, rs2072454, rs2227984, and rs2227983. The PCR fragments were genotyped by single-strand conformation polymorphism (SSCP) method, and each genotype was subjected to direct sequencing. RESULTS: Genotyping experiments confirmed the variability of three targeted variants, and logistic regression analysis showed that two of these variants (rs1050171 and rs2227983) tend to exhibit a significant association with NSCLC. Individuals with rs1050171:GA genotype showed a possible association with the increased risk of NSCLC (P = 0.0110; OD 5.2636; Cl95% 1.4630 to 18.9371). Individuals with rs2227983:GG genotype exhibited a potential association with NSCLC (P = 0.0037; OD 5.2683; Cl95% 1.7141 to 16.1919). Linkage disequilibrium analysis showed that the effects of the investigated variants seem to take independent actions, and no haplotype was found to be associated with the high prevalence of NSCLC. CONCLUSIONS: Our collective data indicated that EGFR-rs1050171G/A and EGFR-rs2227983G/G SNPs tend to exert significant and separate associations with the increased risk of NSCLC. However, this study recommends using a broader spectrum of the investigated samples to get further details of both SNPs in terms of their association with the susceptibility to NSCLC.

Antimicrobial, Antitumor and Side Effects Assessment of a Newly Synthesized Tamoxifen Analog.

BACKGROUND: Tamoxifen citrate is a very prevalent drug marketed under several trade names like Apo-Tamox, Nolvadex, Tamec, Tamizam, and Tamoplex. This molecule is approved by the FDA for breast cancer treatment. Some studies have shown that tamoxifen has anti-tuberculosis and antiparasitic activities. Like any drug, tamoxifen possesses side effects, more or less dangerous. AIMS: Basically, this work is a comparative study that aims to: primarily compare the antimicrobial and antitumor activities of tamoxifen and a newly synthesized tamoxifen analog; and to determine the molecule with lesser side effects. METHODS: Three groups of mice were injected with tamoxifen citrate and compound 2(1,1-bis[4-(3- dimethylaminopropoxy)phenyl]-2-phenyl-but-1-ene dihydrochloride) at doses corresponding to C1 (1/10), C2 (1/50), and C3 (1/100) to compound 2 lethal dose (LD50 = 75 mg/kg) administered to adult mice. A group of noninjected mice served as a study control. RESULTS: Experimental results suggest that compound 2 has better antitumor and antimicrobial activity than tamoxifen citrate besides its lower toxicity effects. CONCLUSION: The results obtained from the present study confirmed the antitumor and antimicrobial effect of tamoxifen citrate and its hematological side effects. Compound 2 seems to be more effective than tamoxifen citrate for antitumor and antimicrobial treatment while having less hematological side effects and less disruption of the blood biochemical parameters. These findings encourage us to perform further studies on compound 2 and test it for other therapeutic uses for which tamoxifen was found effective.

Extraction, characterization and biological properties of polysaccharide derived from green seaweed "Chaetomorpha linum" and its potential application in Tunisian beef sausages.

A novel polysaccharide extracted from green algae Chaetomorpha linum (PS) was characterized, using infrared spectroscopy, HPLC-FID, gel filtration high-pressure chromatography, thin layer chromatography and spectrum visible UV. Natural antioxidant potential of PS was evaluated based on DPPH free radical, ferrous iron-chelating, ß carotene bleaching inhibition activities and DNA nicking assay. Functional properties were estimated based on Water Holding Capacity (WHC), Oil Holding Capacity (OHC), emulsifying activity and foaming ability. Overall, data showed attractive chemical, functional and biological properties with an antioxidant capacity of PS in beef sausages during storage for 12 days. Indeed, as compared to standard formulation (with addition of vitamin C), samples formulated with PS presented lower values in terms of lipid oxidation (TBARS, MetMb), while preserving color properties compared with untreated samples. Furthermore, lower changes in pH, moisture, and the highest values of heme iron were obtained. Successful inhibition of microbial proliferation was proved. Endowed with high antioxidant and antimicrobial activities, PS could thus be used as a natural conservative in functional foods.

Potential benefits of polysaccharides derived from marine alga Ulva lactuca against hepatotoxicity and nephrotoxicity induced by thiacloprid, an insecticide pollutant.

The present study aimed to evaluate the potential protective and antioxidant effect of polysaccharides (PS) extracted from Ulva lactuca against thiacloprid (THC) induced nephrotoxicity and hepatotoxicity. The antioxidant capacity of PS was tested in vitro using ABTS radical scavenging activity and plasmid DNA cleavage assays andin vivo on adult male rats treated for 30 days. Animals were allocated into four groups: control; THC (22.5 mg/kg); THC (22.5 mg/kg) + PS1 (100 mg/kg diet); and THC (22.5 mg/kg) + PS2 (200 mg/kg diet). The structural features of PS were determined by Fourier transformed infrared (FT-IR), UV absorption peak detection, high performance liquid chromatography (HPLC) and gel permeation chromatography, and also functional properties were investigated. Overall, results indicated that THC increased significantly malondialdehyde, advanced oxidation protein products, glutathione levels, which is correlated with severe histological and plasmatic biochemical injuries in both liver and kidney tissues. However, cotreatment PS induced a significant protective and healing affects against the nephrotoxicity and hepatotoxcity induced by THC.

Polysaccharide from a Tunisian red seaweed Chondrus canaliculatus: Structural characteristics, antioxidant activity and in vivo hemato-nephroprotective properties on maneb induced toxicity.

The present study aims to investigate the physicochemical and the structural features of polysaccharide isolated from the red marine macro alga Chondrus canaliculatus (C.C.P) using FT-IR, gel filtration high-pressure chromatograph, HPLC-FID and solid state 13C NMR analysis. C.C.P was even more tested in vitro for its potential antioxidant properties and in vivo for its hemato-nephroprotective effects against fungicide - maneb (MB) - induced toxicity. Animals treated for 20 days were allocated into six groups per six rats each: group 1 served as vehicle control, group 2 received MB, group 3 received MB + C.C.P (100 mg/kg), group 4 MB + C.C.P (200 mg/kg), group 5 and 6 used as a positive control groups receiving only C.C.P; one 100 and the other 200 mg/kg, respectively. After MB injection, our data displayed a significant disruption in all hematological parameters associated with clear signs of nephrotoxicity. However, co-treatment with C.C.P at two graded doses led to an effective healing process against MB's hematological, biochemical, and histological kidney's oxidative injuries. In summary, our data suggest that C.C.P could be a prospective potent antioxidant, nephro and hemato-protective agent.

Cytoprotective Effects of the Red Marine Alga Chondrus canaliculatus Against Maneb-Induced Hematotoxicity and Bone Oxidative Damages in Adult Rats.

The current study aimed at evaluating the ability of a mineral and antioxidant-rich extract from Chondrus canaliculatus to improve maneb (MB)-induced toxicity in adult rat. The animals were divided into four groups: group 1 used as a control group, group 2 received MB, group 3 received MB + C. canaliculatus extract, and group 4 received only the algal extract. MB, a Mn-containing ethylene-bis-dithiocarbamate fungicide, induced oxidative stress damages, mineral perturbations in the plasma, urine, and bone, and genotoxicity in rats. Hematological analysis revealed in the MB-treated group a disruption in the number of red blood cells, platelets, and white blood cells associated with a striking genotoxicity. Interestingly, a significant increase in malondialdehyde and advanced oxidation protein product levels in erythrocytes and bones were found. On the other hand, an impairment of the antioxidant status in both tissues was occurred. Along, our results revealed that MB injection caused a striking drop and disruption in bone's mineral rates, especially calcium and phosphorus. These biochemical results were in accordance with the histological and molecular changes. However, co-treatment with C. canaliculatus extract showed, for the first time, that this alga was effective against MB-induced hematotoxicity, genotoxicity, and oxidative stress in the blood and bone and maintained osteomineral metabolism and bone histo-architecture. Such observations might be explained by the strong in vitro antioxidant and antibacterial activities exhibited by the alga, as well as by its high levels in several minerals: calcium, phosphorus, sodium, potassium, magnesium, iron, and zinc.

Aluminium and Acrylamide Disrupt Cerebellum Redox States, Cholinergic Function and Membrane-Bound ATPase in Adult Rats and Their Offspring.

Accumulation of aluminium and acrylamide in food is a major source of human exposure. Their adverse effects are well documented, but there is no information about the health problems arising from their combined exposure. The aim of the present study was to examine the possible neurotoxic effects after co-exposure of pregnant and lactating rats to aluminium and acrylamide in order to evaluate redox state, cholinergic function and membrane-bound ATPases in the cerebellum of adult rats and their progeny. Pregnant female rats have received aluminium (50 mg/kg body weight) via drinking water and acrylamide (20 mg/kg body weight) by gavage, either individually or in combination from the 14th day of pregnancy until day 14 after delivery. Exposure to these toxicants provoked an increase in malondialdehyde (MDA) and advanced oxidation protein product (AOPP) levels and a decrease in SOD, CAT, GPx, Na+K+-ATPase, Mg2+-ATPase and AChE activities in the cerebellum of mothers and their suckling pups. A reduction in GSH, NPSH and vitamin C levels was also observed. These changes were confirmed by histological results. Interestingly, co-exposure to these toxicants exhibited synergism based on physical and biochemical variables in the cerebellum of mothers and their progeny.

A mineral and antioxidant-rich extract from the red marine Algae Alsidium corallinum exhibits cytoprotective effects against potassium bromate-induced erythrocyte oxidative damages in mice.

The present study was carried out to investigate potassium bromate toxicity in mice and the corrective effects of marine algae Alsidium corallinum. The red algae demonstrated its rich composition in phenols, triterpenes, flavonoids, alkaloids, tropolones, sodium, potassium, calcium, magnesium, iron, copper, and zinc. To confirm its antioxidant potential, an in vivo study was performed on adult mice. The animals were divided into four groups: group I were used as controls, group II received potassium bromate (0.5 g/L) via drinking water, group III received potassium bromate (0.5 g/L) by the same route as group II and 7% of A. corallinum ethanolic extract via their diet, and group IV received only 7% of algae. The potassium bromate-treated group showed a significant decrease in erythrocyte, platelet, hemoglobin, and hematocrit values and a significant increase in total white blood cells, compared to those of controls. While, superoxide dismutase, catalase, glutathione, and vitamin C values were decreased by potassium bromate treatment, lipid peroxidation (as malondialdehyde) and erythrocyte osmotic fragility values were increased. Interestingly, potassium bromate treatment showed significant genotoxic effects, as demonstrated by DNA degradation. These changes were confirmed by blood smears histopathological observations which were marked by a necrosis and a decrease of erythrocytes number. A. corallinum extract appeared to be effective against hematotoxic and genotoxic changes induced by potassium bromate, as evidenced by the improvement of the parameters cited above.

Oxidative stress-related lung dysfunction by chromium(VI): alleviation by Citrus aurantium L

Chromium(VI), a very strong oxidant, causes high cytotoxicity through oxidative stress in tissue systems. Our study investigated the potential ability of ethanolic Citrus aurantium L., family Rutaceae extract, used as a nutritional supplement, to alleviate lung oxidative damage induced by Cr(VI). A high-performance liquid chromatography coupled with a mass spectrometer method was developed to separate and identify flavonoids in C. aurantium L. Six flavonoids were identified, as (1) poncirin, (2) naringin, (3) naringenin, (4) quercetin, (5) isosinensetin, and (6) tetramethyl-o-isoscutellarein. Adult Wistar rats, used in this study, were divided into six groups of six animals each: group I served as controls which received standard diet, group II received via drinking water K2Cr2O7 alone (700 ppm), groups III and IV were pretreated for 10 days with ethanol extract of C. aurantium L. at doses of 100 and 300 mg/kg body weight/day, respectively, and then K2Cr2O7 was administrated during 3 weeks, and groups V and VI received during 10 days only C. aurantium L. ethanol extract at doses of 100 and 300 mg/kg/day, respectively. Ethanol extract of C. aurantium L. was administered orally. Rats exposed to Cr(VI) showed in lung an increase in malondialdehyde and protein carbonyl levels and a decrease in sulflydryl content, glutathione, nonprotein thiol, and vitamins C and E levels. Decreases in enzyme activities such as in Na+K+ ATPase, catalase, glutathione peroxidase, and superoxide dismutase were noted. Pretreatment with C. aurantium L. of chromium-treated rats ameliorated all biochemical parameters. Lung histological studies confirmed the biochemical parameters and the beneficial role of C. aurantium L (AU)

Protective effects of vitamin E and selenium against dimethoate-induced cardiotoxicity in vivo: biochemical and histological studies.

There is considerable interest in the study of free radical-mediated damage to biological systems due to pesticide exposure. However, there is a lack of consensus as to which determinations are best used to quantify future risks arising from xenobiotic exposure and natural antioxidant interventions. Our study investigated the potential ability of selenium and/or vitamin E, used as nutritional supplements, to alleviate cardiotoxicity induced by dimethoate. Female Wistar rats were exposed for 30 days either to dimethoate (0.2 g L⁻¹ of drinking water), dimethoate+selenium (0.5 mg kg⁻¹ of diet), dimethoate+vitamin E (100 mg kg⁻¹ of diet), or dimethoate+selenium+vitamin E. The exposure of rats to dimethoate promoted oxidative stress with a rise in malondialdehyde, advanced protein oxidation, and protein carbonyl levels. An increase of glutathione peroxidase, superoxide dismutase, and catalase activities was also noted. A fall in acetylcholinesterase and Na⁺ K⁺-ATPase activities, glutathione, nonprotein thiols, vitamins C and E levels was observed. Plasma levels of cholesterol, triglycerides, and low density lipoprotein-cholesterol increased and those of high density lipoprotein-cholesterol decreased. Coadministration of selenium or vitamin E to the diet of dimethoate-treated rats ameliorated the biochemical parameters cited above. The histopathological findings confirmed the biochemical results and the potential protective effects of selenium and vitamin E against cardiotoxicity induced by dimethoate.

Ameliorating effect of selenium on chromium (VI)-induced oxidative damage in the brain of adult rats

Chromium is known for its wide toxic manifestations. This experiment aims to evaluate the effect of selenium against oxidative stress induced by chromium in the cerebrum and cerebellum. Female Wistar rats were randomly divided into four groups of six each: group I served as controls which received the standard diet; group II received drinking water K2Cr2O7 alone (700 ppm); group III received both K2Cr2O7 and Se (0.5 mg Na2SeO3/kg of diet); and group IV received Se (0.5 mg/kg of diet) for 3 weeks. The exposure of rats to K2Cr2O7 promoted oxidative stress in the cerebrum and cerebellum with an increase in malondialdehyde and a decrease of nonenzymatic antioxidant levels such as glutathione, nonprotein thiol, and vitamin C. An increase of enzyme activities like catalase, glutathione peroxidase, and superoxide dismutase activities was also observed. Acetylcholinesterase activity was inhibited after treatment with K2Cr2O7. Co-administration of Se restored the parameters cited above. The histopathological findings confirmed the biochemical results (AU)

Dimethoate induced oxidative damage and histopathological changes in lung of adult rats: modulatory effects of selenium and/or vitamin E.

OBJECTIVE: To determine the efficiency of selenium and/or vitamin E to alleviate lung oxidative damage induced by dimethoate, an organophosphorus compound. METHODS: Adult Wistar rats were exposed during 30 days either to dimethoate (0.2 g/L of drinking water), dimethoate+selenium (0.5 mg/kg of diet), dimethoate+vitamin E (100 mg/kg of diet), or dimethoate+selenium+vitamin E. RESULTS: Exposure to dimethoate caused oxidative stress in lung evidenced by an increase of malondialdehyde, protein carbonyl groups and advanced oxidation protein products. An increase in glutathione peroxidase, superoxide dismutase, catalase and a decrease in acetylcholinesterase and butyrylcholinesterase activities, glutathione, non-protein thiols and vitamins C levels were observed. Histopathological changes in lung tissue were noted as emphysema, hemorrhages and hemosiderin deposits. Co-administration of selenium or vitamin E to the diet of dimethoate treated rats ameliorated the biochemical parameters as well as histological impairments. The joint effect of these elements was more powerful in antagonizing dimethoate-induced lung oxidative damage. CONCLUSION: We concluded that selenium and vitamin E ameliorated the toxic effects of this pesticide in lung tissue suggesting their role as potential antioxidants.

Ameliorating effect of selenium on chromium (VI)-induced oxidative damage in the brain of adult rats.

Chromium is known for its wide toxic manifestations. This experiment aims to evaluate the effect of selenium against oxidative stress induced by chromium in the cerebrum and cerebellum. Female Wistar rats were randomly divided into four groups of six each: group I served as controls which received the standard diet; group II received drinking water K(2)Cr(2)O(7) alone (700 ppm); group III received both K(2)Cr(2)O(7) and Se (0.5 mg Na(2)SeO(3)/kg of diet); and group IV received Se (0.5 mg/kg of diet) for 3 weeks. The exposure of rats to K(2)Cr(2)O(7) promoted oxidative stress in the cerebrum and cerebellum with an increase in malondialdehyde and a decrease of nonenzymatic antioxidant levels such as glutathione, nonprotein thiol, and vitamin C. An increase of enzyme activities like catalase, glutathione peroxidase, and superoxide dismutase activities was also observed. Acetylcholinesterase activity was inhibited after treatment with K(2)Cr(2)O(7). Co-administration of Se restored the parameters cited above. The histopathological findings confirmed the biochemical results.

Oxidative damage in erythrocytes of adult rats and their suckling pups exposed to gibberellic acid.

Gibberellic acid (GA(3)) is a plant growth regulator used in agriculture worldwide. The present study investigated the propensity of GA(3) to induce hematological disorders. Pregnant Wistar rats were randomly divided into two groups: group I served as controls; group II received orally GA(3) (200 ppm) from the 14th day of pregnancy until day 14 after delivery. GA(3) reduced the number of red blood cells, hemoglobin concentration, and hematocrit in suckling rats, while these parameters remained unchanged in their mothers. White blood cells increased in mothers and were unchanged in their pups. Several studies have associated these hematological disorders with oxidative stress. In fact, GA(3) treatment revealed in erythrocytes a significant increase in malondialdehyde levels and a decrease in antioxidant enzyme activities such as superoxide dismutase, catalase, and glutathione peroxidase. Moreover, a significant decline was observed in acetylcholinesterase activity, glutathione, nonprotein thiols, and vitamin C levels.

Oxidative damage induced by chromium (VI) in rat erythrocytes: protective effect of selenium

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Excess chromium (Cr) exposure is associated with various pathological conditions including hematological dysfunction. The generation of oxidative stress is one of the plausible mechanisms behind Cr-induced cellular deteriorations. The efficacy of selenium (Se) to combat Cr-induced oxidative damage in the erythrocytes of adult rats was investigated in the current study. Female Wistar rats were randomly divided into four groups of six each: group I served as controls which received standard diet, group II received in drinking water K2Cr2O7 alone (700 ppm), group III received both K2Cr2O7 and Se (0.5 Na2SeO3 mg/kg of diet), and group IV received Se (0.5 mg/kg of diet) for 3 weeks. Rats exposed to K2Cr2O7 showed an increase of malondialdehyde and protein carbonyl levels and a decrease of sulfhydryl content, glutathione, non-protein thiol, and vitamin C levels. A decrease of enzyme activities like catalase, glutathione peroxidase, and superoxide dismutase activities was also noted. Co-administration of Se with K2Cr2O7 restored the parameters cited above to near-normal values. Therefore, our investigation revealed that Se was a useful element preventing K2Cr2O7-induced erythrocyte damages (AU)

Oxidative stress and thyroid impairment after gibberellic acid treatment in pregnant and lactating rats and their offspring.

Gibberellic acid (GA3) has been worldwide used in agriculture as a plant growth regulator. The purpose of this study is to assess the effects of GA3 on the morphology and the thyroid hormone levels in adult rats and their suckling pups. Animals were given daily 200 ppm GA3 in drinking water from the 14th day of pregnancy until day 14 after delivery. Compared with a control group, GA3-treated mothers and pups showed an increase in body and thyroid weights, a decrease in plasma FT4 and FT3 levels, which were more pronounced in pups than in their mothers. Thyroid iodine content was also decreased in pups. These biochemical modifications corresponded histologically; the majority of follicles had cubical epithelial cells, which surrounded empty vesicular cavities. Toxicity was objectified by a significant increase in plasma malondialdehyde, protein carbonyls, and advanced oxidation protein products levels in GA3-treated dams and their suckling pups; while, the activities of superoxide dismutase, catalase, and glutathione peroxidase were decreased in plasma of both dams and their pups. Moreover, a significant decline was observed in plasma glutathione, nonprotein thiols, and vitamin C levels. We conclude that GA3 treatment affects thyroid function and plasma antioxidant status in adult rats and their progeny.

Oxidative stress induced by gibberellic acid on kidney tissue of female rats and their progeny: biochemical and histopathological studies

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Gibberellic acid (GA3) is an endogenous plant growth regulator used worldwide in agriculture. The objective of this study was to investigate the effects of GA3 on the kidney function of adult rats and their pups. Female Wistar rats were given daily 200 ppm GA3 in drinking water from the 14th day of pregnancy until day 14 after delivery. GA3 induced nephrotoxicity, as evidenced by a reduction in the 24-h urine volume and an increase in plasma creatinine, urea and uric acid levels. Nephrotoxicity was objectified by a significant increase of malondialdehyde level and a decrease of antioxidant enzyme activities like catalase, superoxide dismutase, glutathione peroxidase and glutathione content in kidneys of suckling pups and their mothers. Kidney histological studies confirmed biochemical parameters. We concluded that the exposure of rats to GA3 induced oxidative stress and histopathological changes in kidneys of suckling rats and their mothers during late pregnancy and early postnatal periods (AU)

Protective effects of selenium on methimazole-induced anemia and oxidative stress in adult rats and their offspring.

The present study investigates the potential ability of selenium, considered as an antioxidant with pharmacological property to alleviate oxidative stress and hematological parameter disorders induced by methimazole, an antithyroid drug. Pregnant Wistar rats were randomly divided into four groups of six each: group I served as negative control and received a standard diet; group II received 250 mg/L of methimazole in drinking water and a standard diet; group III received both methimazole (250 mg/L, orally) and selenium (0.5 mg/kg of diet) supplemented to the standard diet; group IV served as positive control and received a supplement of selenium in the diet (0.5 mg/kg of diet) as sodium selenite (Na(2)SeO(3)). Treatment was started from the 14th day of pregnancy until day 14 after delivery. Methimazole reduced the number of red blood cells, hemoglobin concentration and hematocrit in mothers and their pups. Besides, plasma iron, vitamins B(9), B(12), C and E levels were reduced. Lipid peroxidation increased, objectified by high malondialdehyde levels and lactate dehydrogenase activity in plasma, while glutathione, glutathione peroxidase, superoxide dismutase and catalase activities showed a significant decline. Co-administration of selenium through diet improved all the parameters cited above. It can be concluded that the administration of selenium alleviates methimazole-induced toxicity, thus demonstrating its antioxidant efficacy.