Displaying publications 21 - 30 of 30 in total

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  1. Saad B, Ariffin M, Saleh MI
    Talanta, 1998 Dec;47(5):1231-6.
    PMID: 18967428
    A flow injection potentiometric method for the rapid determination of paraquat in herbicide formulations and biological samples is described. It is based on the utilization of a flow-through potentiometric detector containing polyvinyl chloride-immobilised octamethylcyclotetrasiloxane, a lipophilic plasticizer (tetra-n-undecyl 3,3',4,4'-benzophenone tetracarboxylate) and membrane additive potassium tetrakis(4-chlorophenyl)borate. The detector was minimally interfered by the presence of constituents such as Na(+), K(+), Ca(2+), Mg(2+), glucose, urea, lactic and citric acids at physiological levels, respectively. Good correlation between results of the proposed method and HPLC for the formulation samples was found, while results for the determination of paraquat in biological samples such as urine, vomitus and stomach washout was less satisfactory.
    Matched MeSH terms: Paraquat
  2. Farah Wahida Ibrahim, Umi Noraashikin Zainudin, Mazlyzam Abdul Latif, Asmah Hamid
    Sains Malaysiana, 2018;47:2337-2347.
    Zingiber zerumbet has been traditionally used as an anti-inflammation and antioxidant agent. The present study
    investigates the neuroprotective effects of ethyl acetate extract of Z. zerumbet against oxidative stress on paraquat
    (PQ)-induced Parkinsonism in rats. Forty male Sprague-Dawley rats were divided into five groups: Negative control
    (normal saline), positive control (N-acetylcysteine, NAC 20 mg/kg + PQ 10 mg/kg), PQ only, 200 mg/kg Z. zerumbet +
    PQ and 400 mg/kg Z. zerumbet + PQ. The extract was given orally for 19 consecutive days and PQ was administered
    intraperitoneally on day 8-12th of the treatment regime. Both serum and fresh brains containing substantia nigra (SN)
    region were taken for biochemical and histological analysis. Administration of both 200 and 400 mg/kg ethyl acetate
    Z. zerumbet extracts to the PQ-treated groups have resulted in: Decreased levels of MDA and PC in the SN homogenates;
    and increased SOD, GPx; and CAT activities in the SN and serum. Overall, ethyl acetate extract of Z. zerumbet reduced
    oxidative stress in the SN of PQ-induced neuronal damages, therefore, has the potential to be developed as a preventive
    agent for neurodegenerative disorders caused by environmental toxins.
    Matched MeSH terms: Paraquat
  3. Koh KH, Tan CH, Hii LW, Lee J, Ngu LL, Chai AJ, et al.
    Toxicol Rep, 2014;1:490-495.
    PMID: 28962262 DOI: 10.1016/j.toxrep.2014.06.010
    Paraquat poisoning resulted in multiorgan failure and is associated with high mortality. We audited 83 historical cases of paraquat poisoning in past 2 years treated with conventional decontamination and supportive treatment, followed by enrolling 85 patients over a 2 year period into additional immunosuppression with intravenous (i.v.) methylprednisolone and i.v. cyclophosphamide. Our results showed that age, poor renal function and leucocytosis are the main predictors of fatal outcome. Immunosuppression regime rendered higher survival (6 out of 17 patients (35.3%)) versus historical control (1 out of 18 patients (5.6%)) (p = 0.041) in the cohort with admission eGFR < 50 ml/min/1.73 m(2) and WBC count > 11,000/μL. In contrast, there was no difference in survival with immunosuppression regime (38 out of 64 patients (59.4%)) compared to historical control (30 out of 52 patients (57.7%)) (p = 0.885) in those with eGFR > 50 ml/min/1.73 m(2) or WBC < 11,000/μL at presentation. Multivariable logistic regression showed survival probability = exp(logit)/(1 + exp(logit)), in which logit = 13.962 - (0.233 × ln(age (year))) - (1.344 × ln(creatinine (μmol/L))) - (1.602 × ln(rise in creatinine (μmol/day))) - (0.614 × ln(WBC (,000/μL))) + (2.021 × immunosuppression) and immunosuppression = 1 if given and 0 if not. Immunosuppression therapy yielded odds ratio of 0.132 (95% confidential interval: 0.029-0.603, p = 0.009). In conclusion, immunosuppression therapy with intravenous methylprednisolone and cyclophosphamide may counteract immune mediated inflammation after paraquat poisoning and improve survival of patients with admission eGFR < 50 ml/min/1.73 m(2) and WBC count > 11,000/μL.
    Matched MeSH terms: Paraquat
  4. Baharuddin MR, Sahid IB, Noor MA, Sulaiman N, Othman F
    J Environ Sci Health B, 2011;46(7):600-7.
    PMID: 21749249 DOI: 10.1080/03601234.2011.589309
    A cross-section analytical study was conducted to evaluate the risk of pesticide exposure to those applying the Class II pesticides 2,4-D and paraquat in the paddy-growing areas of Kerian, Perak, Malaysia. It investigated the influence of weather on exposure as well as documented health problems commonly related to pesticide exposure. Potential inhalation and dermal exposure for 140 paddy farmers (handlers of pesticides) were assessed. Results showed that while temperature and humidity affected exposure, windspeed had the strongest impact on pesticide exposure via inhalation. However, the degree of exposure to both herbicides via inhalation was below the permissible exposure limits set by United States National Institute of Occupational Safety and Health (NIOSH). Dermal Exposure Assessment Method (DREAM) readings showed that dermal exposure with manual spraying ranged from moderate to high. With motorized sprayers, however, the level of dermal exposure ranged from low to moderate. Dermal exposure was significantly negatively correlated with the usage of protective clothing. Various types of deleterious health effects were detected among users of manual knapsack sprayers. Long-term spraying activities were positively correlated with increasing levels of the gamma-glutamyl transpeptidase (GGT) liver enzyme. The type of spraying equipment, usage of proper protective clothing and adherence to correct spraying practices were found to be the most important factors influencing the degree of pesticide exposure among those applying pesticides.
    Matched MeSH terms: Paraquat/toxicity*
  5. D'Souza UJ, Narayana K, Zain A, Raju S, Nizam HM, Noriah O
    Folia Morphol (Warsz), 2006 Feb;65(1):6-10.
    PMID: 16783728
    The effects of exposure to low doses of paraquat, a herbicide, via the dermal route were studied on the spermatozoa of Sprague-Dawley rats. Paraquat (1, 1'-dimethyl-4, 4'-bipyridinium dichloride) was administered once a day for five days, at intervals of 24 h at 0, 6, 15 and 30 mg/kg, and the rats were sacrificed on days 7, 14, 28, and 42 after the last exposure. The sperm suspensions were obtained by mincing the caudae epididymes and ductus deferens for the purpose of performing a sperm morphology test, sperm count and analysis of sperm mortality and sperm motility, as per the standard procedures. The sperm count was decreased (p < 0.05) only on days 7 and 14 but sperm abnormalities increased on all days (p < 0.05). Sperm mortality increased at higher dose-levels (p < 0.05) except on day 42, and motility was affected by 30 mg/kg only on day 42. In conclusion, paraquat is a genotoxic and cytotoxic agent to germ cells in the male rat.
    Matched MeSH terms: Paraquat/toxicity*
  6. Howard JK
    Br J Ind Med, 1979 Aug;36(3):220-3.
    PMID: 500781
    A group of 18 male Caucasian workers from the United Kingdom and a further group of 18 male mixed race (mainly Malay) workers from Malaysia employed in the formulation of paraquat-based herbicides were examined for evidence of chronic ill health after long-term exposure to paraquat. Clinical records were examined, medical and occupational histories were obtained and a clinical examination, particularly of the skin, was undertaken. Skin rashes, nail damage and epistaxes were encountered by most workers as a result of direct contact of skin and mucous membranes with paraquat. These conditions subsided rapidly and no worker reported any sequelae. There was no clinical evidence of long-term effects on skin, mucous membranes or general health following exposure to paraquat over several years in these workers.
    Matched MeSH terms: Paraquat/adverse effects*
  7. El-Gamal M, Salama M, Collins-Praino LE, Baetu I, Fathalla AM, Soliman AM, et al.
    Neurotox Res, 2021 Jun;39(3):897-923.
    PMID: 33765237 DOI: 10.1007/s12640-021-00356-8
    Parkinson's disease (PD), the second most common neurodegenerative disorder, is characterized by cardinal motor impairments, including akinesia and tremor, as well as by a host of non-motor symptoms, including both autonomic and cognitive dysfunction. PD is associated with a death of nigral dopaminergic neurons, as well as the pathological spread of Lewy bodies, consisting predominantly of the misfolded protein alpha-synuclein. To date, only symptomatic treatments, such as levodopa, are available, and trials aiming to cure the disease, or at least halt its progression, have not been successful. Wong et al. (2019) suggested that the lack of effective therapy against neurodegeneration in PD might be attributed to the fact that the molecular mechanisms standing behind the dopaminergic neuronal vulnerability are still a major scientific challenge. Understanding these molecular mechanisms is critical for developing effective therapy. Thirty-five years ago, Calne and William Langston (1983) raised the question of whether biological or environmental factors precipitate the development of PD. In spite of great advances in technology and medicine, this question still lacks a clear answer. Only 5-15% of PD cases are attributed to a genetic mutation, with the majority of cases classified as idiopathic, which could be linked to exposure to environmental contaminants. Rodent models play a crucial role in understanding the risk factors and pathogenesis of PD. Additionally, well-validated rodent models are critical for driving the preclinical development of clinically translatable treatment options. In this review, we discuss the mechanisms, similarities and differences, as well as advantages and limitations of different neurotoxin-induced rat models of PD. In the second part of this review, we will discuss the potential future of neurotoxin-induced models of PD. Finally, we will briefly demonstrate the crucial role of gene-environment interactions in PD and discuss fusion or dual PD models. We argue that these models have the potential to significantly further our understanding of PD.
    Matched MeSH terms: Paraquat/toxicity
  8. Hossain F, Ali O, D'Souza UJ, Naing DK
    J Occup Health, 2010;52(6):353-60.
    PMID: 20924153
    OBJECTIVES: To determine the relationship between semen quality and exposure to pesticide residues.

    METHODS: A cross-sectional study was conducted among male farmers from 3 different communities in Sabah, Malaysia. A total of 152 farmers participated in this study of whom 62 farmers had been exposed to either paraquat or malathion or both to varying extents. Questionnaires were designed to record a history of pesticides exposure and other potential risk factors among farmers. All semen samples were collected, processed and analyzed by qualified personnel based on WHO guidelines. Volume, pH, sperm concentration, motility, morphology and WBC count were examined and recorded. The association between pesticide exposure and semen parameters was highly significant.

    RESULTS: The mean values of volume, pH, sperm concentration, motility, and WBC count were significantly less in the exposed group than in compared with the non-exposed group, with p<0.005. Those who were exposed to pesticides had greater risk of having abnormal semen parameters than those in with the non exposed group, with p values of less than 0.05. The comparison between semen qualities such as lower sperm count, motility and higher percentage of sperm abnormality of those exposed to different types of pesticides (paraquat and malathion) showed no significant differences.

    CONCLUSION: The results showed a significant decline in semen quality with a decline in sperm count, motility and higher percent of teratospermia among subjects with pesticide exposure, and those who were exposed to pesticides had significantly 3 to 9 times greater risk of having abnormal semen parameters.

    Matched MeSH terms: Paraquat/adverse effects*
  9. Idris ZHC, Abidin AAZ, Subki A, Yusof ZNB
    Trop Life Sci Res, 2018 Mar;29(1):71-85.
    PMID: 29644016 MyJurnal DOI: 10.21315/tlsr2018.29.1.5
    Thiamine is known to be an important compound in human diet and it is a cofactor required for vital metabolic processes such as acetyl-CoA biosynthesis, amino acid biosynthesis, Krebs and Calvin cycle. Besides that, thiamine has been shown to be involved in plant protection against stress. In this study, the level of expression of THIC and THI1/THI4, the genes for the first two enzymes in the thiamine biosynthesis pathway were observed when oil palm (Elaeis guineensis) was subjected to oxidative stress. Primers were designed based on the consensus sequence of thiamine biosynthesis genes obtained from Arabidopsis thaliana, Zea mays, Oryza sativa, and Alnus glutinosa. Oxidative stress were induced with various concentrations of paraquat and samplings were done at various time points post-stress induction. The expression of THIC and THI1/THI4 genes were observed via RT-PCR and qPCR analysis. The expression of THIC was increased 2-fold, while THI1/THI4 gene transcript was increased 4-fold upon induction of oxidative stress. These findings showed that oil palm responded to oxidative stress by over-expressing the genes involved in thiamine biosynthesis. These findings support the suggestion that thiamine may play an important role in plant protection against stress.
    Matched MeSH terms: Paraquat
  10. Ng YW, Say YH
    PeerJ, 2018;6:e4696.
    PMID: 29713567 DOI: 10.7717/peerj.4696
    Background: Obesity-related central nervous system (CNS) pathologies like neuroinflammation and reactive gliosis are associated with high-fat diet (HFD) related elevation of saturated fatty acids like palmitic acid (PA) in neurons and astrocytes of the brain.

    Methods: Human neuroblastoma cells SH-SY5Y (as a neuronal model) and human glioblastoma cells T98G (as an astrocytic model), were treated with 100-500 µM PA, oleic acid (OA) or lauric acid (LA) for 24 h or 48 h, and their cell viability was assessed by 3-(4,5-dimetylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The effects of stable overexpression of γ-synuclein (γ-syn), a neuronal protein recently recognized as a novel regulator of lipid handling in adipocytes, and transient overexpression of Parkinson's disease (PD) α-synuclein [α-syn; wild-type (wt) and its pathogenic mutants A53T, A30P and E46K] in SH-SY5Y and T98G cells, were also evaluated. The effects of co-treatment of PA with paraquat (PQ), a Parkinsonian pesticide, and leptin, a hormone involved in the brain-adipose axis, were also assessed. Cell death mode and cell cycle were analyzed by Annexin V/PI flow cytometry. Reactive oxygen species (ROS) level was determined using 2',7'-dichlorofluorescien diacetate (DCFH-DA) assay and lipid peroxidation level was determined using thiobarbituric acid reactive substances (TBARS) assay.

    Results: MTT assay revealed dose- and time-dependent PA cytotoxicity on SH-SY5Y and T98G cells, but not OA and LA. The cytotoxicity was significantly lower in SH-SY5Y-γ-syn cells, while transient overexpression of wt α-syn or its PD mutants (A30P and E46K, but not A53T) modestly (but still significantly) rescued the cytotoxicity of PA in SH-SY5Y and T98G cells. Co-treatment of increasing concentrations of PQ exacerbated PA's neurotoxicity. Pre-treatment of leptin, an anti-apoptotic adipokine, did not successfully rescue SH-SY5Y cells from PA-induced cytotoxicity-suggesting a mechanism of PA-induced leptin resistance. Annexin V/PI flow cytometry analysis revealed PA-induced increase in percentages of cells in annexin V-positive/PI-negative quadrant (early apoptosis) and subG0-G1 fraction, accompanied by a decrease in G2-M phase cells. The PA-induced ROS production and lipid peroxidation was at greater extent in T98G as compared to that in SH-SY5Y.

    Discussion: In conclusion, PA induces apoptosis by increasing oxidative stress in neurons and astrocytes. Taken together, the results suggest that HFD may cause neuronal and astrocytic damage, which indirectly proposes that CNS pathologies involving neuroinflammation and reactive gliosis could be prevented via the diet regimen.

    Matched MeSH terms: Paraquat
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