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Biomedical subjects

N Ahmad

Publications and source records attributed to N Ahmad.

At least 73 records · Page 4Linked to original sources

Limited heterogeneity of HIV type 1 in infected mothers correlates with lack of vertical transmission.

The human immunodeficiency virus type 1 (HIV-1) envelope V3 region sequences of peripheral blood mononuclear cell DNA were analyzed from three nontransmitting mothers (infected mothers who failed to transmit HIV-1 to their infants in the absence of antiretroviral therapy), including one mother with two deliveries, and compared with the sequences of seven previously analyzed transmitting mothers. The coding potential of the envelope open reading frame, including several patient-specific amino acid motifs and previously described molecular features across the V3 region, were highly conserved. There was a low degree of heterogeneity within the sequences of each nontransmitting mother compared with the sequences of transmitting mothers. In addition, the estimates of genetic diversity of nontransmitting mother sequences were significantly lower compared with transmitting mother sequences. Phylogenetic analysis showed that the sequences of each nontransmitting mother formed distinct clusters that were well discriminated from each other and the sequences of seven transmitting mothers. In conclusion, a low degree of HIV-1 genetic heterogeneity in these infected mothers correlates with lack of vertical transmission; this finding may be useful in developing strategies for further prevention of maternal-fetal transmission.

Amino Acid Sequence↗

Chemoprevention of prostate carcinogenesis by alpha-difluoromethylornithine in TRAMP mice.

Development of effective chemopreventive agents for human consumption requires conclusive evidence of their efficacy in animal models that have relevance to human diseases. Transgenic adenocarcinoma mouse prostate (TRAMP) is an excellent model of prostate cancer that mimics progressive forms of human disease inasmuch as 100% of males develop histological PIN by 8-12 weeks of age that progress to adenocarcinoma with distant site metastases by 24-28 weeks of age. In these animals, ornithine decarboxylase (ODC) activity (>3-fold) as well as protein expression (>4-fold) was found to be markedly higher in the dorsolateral prostate as compared with the nontransgenic littermates, suggesting their suitability to determine the chemopreventive effect of alpha-difluoromethylornithine (DFMO), an enzyme-activated irreversible inhibitor of ODC, against prostate cancer. Using male TRAMP mice, we studied the effect of oral consumption of DFMO on development of prostate carcinogenesis and surrogate end point biomarkers related to prostate cancer progression. In two independent experiments, each consisting of 8 animals on test, the cumulative incidence of prostatic cancer development at 28 weeks of age in 16 untreated TRAMP mice was 100% (16 of 16), whereas 94% (15 of 16) and 69% (11 of 16) of the animals exhibited distant site metastases to lymph nodes and lungs, respectively. Oral consumption of 1% DFMO (w/v) in the drinking water to TRAMP mice from 8 to 28 weeks of age resulted in a significant decrease in (a) weight (59%) and volume (66%) of prostate, (b) genitourinary weight (63%), and (c) ODC enzyme activity (52%) in the dorsolateral prostate. Importantly, in none of the DFMO-fed TRAMP mice were any distant metastases to lymph node and lungs observed. Furthermore, DFMO treatment resulted in the marked reduction in the protein expression of proliferation cell nuclear antigen, ODC, and probasin in the dorsolateral prostate. The protein expression of antimetastases markers, i.e., E-cadherin and alpha- and beta-catenin, was found to be restored in DFMO-fed animals as compared with the non-DFMO-fed mice. These chemopreventive effects of DFMO were further confirmed by immunohistochemical analysis of the dorsolateral prostate. Histological analysis of the dorsolateral prostate of DFMO-fed animals displayed marginal epithelial stratification, a small number of cribriform structures, elongated hyperchromatic epithelial nuclei, and a significant increase in apoptotic index. Non-DFMO-fed animals, on the other hand, displayed extensive epithelial stratification with profound cribriform structures accompanied with marked thickening, remodeling, and hypercellularity of the fibromuscular stroma. In nontransgenic littermates fed with DFMO, no significant alterations in the above parameters were evident. These data demonstrate that ODC represents a promising and rational target for chemoprevention of human prostate cancer and that TRAMP mice are excellent models for screening of novel drugs and chemopreventive regimens for potential human use.

Adenocarcinoma↗

Cell cycle dysregulation by green tea polyphenol epigallocatechin-3-gallate.

Epidemiological, in vitro cell culture, and in vivo animal studies have shown that green tea or its constituent polyphenols, particularly its major polyphenol epigallocatechin-3-gallate (EGCG) may protect against many cancer types. In earlier studies, we showed that green tea polyphenol EGCG causes a G0/G1-phase cell cycle arrest and apoptosis of human epidermoid carcinoma (A431) cells. We also demonstrated that these effects of EGCG may be mediated through the inhibition of nuclear factor kappa B that has been associated with cell cycle regulation and cancer. In this study, employing A431 cells, we provide evidence for the involvement of cyclin kinase inhibitor (cki)-cyclin-cyclin-dependent kinase (cdk) machinery during cell cycle deregulation by EGCG. As shown by immunoblot analysis, EGCG treatment of the cells resulted in significant dose- and time-dependent (i) upregulation of the protein expression of WAF1/p21, KIP1/p27, p16 and p18, (ii) downmodulation of the protein expression of cyclin D1, cdk4 and cdk6, but not of cyclin E and cdk2, (iii) inhibition of the kinase activities associated with cyclin E, cyclin D1, cdk2, cdk4 and cdk6. Taken together, our study suggests that EGCG causes an induction of G1-phase ckis, which inhibit the cyclin-cdk complexes operative in G0/G1 phase of the cell cycle thereby causing a G0/G1-phase arrest of the cell cycle, which is an irreversible process ultimately resulting in an apoptotic cell death. We suggest that the naturally occurring agents such as green tea polyphenols which may inhibit cell cycle progression could be developed as potent anticancer agents for the management of cancer.

Apoptosis↗

Effect of buffering systems on post-thaw motion characteristics, plasma membrane integrity, and acrosome morphology of buffalo spermatozoa.

This study was carried out to identify the suitable buffer for cryopreservation of buffalo semen. Semen was collected with artificial vagina (42 degrees C) from four buffalo bulls. Split pooled ejaculates (n=5), possessing more than 60% visual sperm motility, were extended at 37 degrees C either in tri-sodium citrate (CITRATE), Tris-citric acid (TCA), Tris-Tes (TEST) or Tris-Hepes (HEPEST). Semen was cooled to 4 degrees C in 2 h, equilibrated at 4 degrees C for 4 h, filled in 0.5 ml straws and frozen in a programmable cell freezer before plunging into liquid nitrogen. Thawing of frozen semen was performed after 24 h at 37 degrees C for 15 s. Sperm motion characteristics, plasma membrane integrity, and acrosome morphology of each semen sample were assessed by using computer-assisted semen analyzer (CASA), hypo-osmotic swelling (HOS) assay, and phase-contrast microscope, respectively. Analysis of variance revealed that percent post-thaw visual motility tended (P=0.07) to be higher in HEPEST (61.0+/-2.9) and lowest in CITRATE (48.0+/-2.5). Computerized motility did not vary due to buffering system. Percent post-thaw linear motility tended (P=0.09) to be higher in TCA (78.2+/-5.5) and lower in TEST (52.0+/-6.9). Circular motility (%) was significantly lower (P<0.05) in TCA (11.6+/-2.8) and higher in TEST (29.8+/-5.6). Curvilinear velocity (microm s(-1)) was lower (P<0.05) in TCA (69.4+/-2.0) than in CITRATE (79.0+/-5.8), TEST (87. 2+/-1.6) and HEPEST (82.6+/-3.0). Lateral head displacement (microm) was lowest (P<0.05) in TCA (1.7+/-0.2) and highest in TEST (3.7+/-0. 6). Plasma membrane integrity and normal acrosomes of buffalo spermatozoa did not differ due to buffering system and averaged 40. 0+/-2.7% and 61.4+/-4.6%, respectively. Based upon lower circular motility, curvilinear velocity, and lateral head displacement, it is concluded that post-thaw quality of buffalo semen can be improved using the Tris-TCA buffering system.

Acrosome↗

Green tea polyphenol epigallocatechin-3-gallate differentially modulates nuclear factor kappaB in cancer cells versus normal cells.

Green tea has shown remarkable anti-inflammatory and cancer chemopreventive effects in many animal tumor bioassays, cell culture systems, and epidemiological studies. Many of these biological effects of green tea are mediated by epigallocatechin 3-gallate (EGCG), the major polyphenol present therein. We have earlier shown that EGCG treatment results in apoptosis of several cancer cells, but not of normal cells (J. Natl. Cancer Inst. 89, 1881-1886 (1997)). The mechanism of this differential response of EGCG is not known. In this study, we investigated the involvement of NF-kappaB during these differential responses of EGCG. EGCG treatment resulted in a dose-dependent (i) inhibition of cell growth, (ii) G0/G1-phase arrest of the cell cycle, and (iii) induction of apoptosis in human epidermoid carcinoma (A431) cells, but not in normal human epidermal keratinocytes (NHEK). Electromobility shift assay revealed that EGCG (10-80 microM) treatment results in lowering of NF-kappaB levels in both the cytoplasm and nucleus in a dose-dependent manner in both A431 cells and NHEK, albeit at different concentrations. EGCG treatment was found to result in a dose-based differential inhibition of TNF-alpha- and LPS-mediated activation of NF-kappaB in these cells. The inhibition of NF-kappaB constitutive expression and activation in NHEK was observed only at high concentrations. The immunoblot analysis also demonstrated a similar pattern of inhibition of the constitutive expression as well as activation of NF-kappaB/p65 nuclear protein. This inhibition of TNF-alpha-caused NF-kappaB activation was mediated via the phosphorylative degradation of its inhibitory protein IkappaBalpha. Taken together, EGCG was found to impart differential dose-based NF-kappaB inhibitory response in cancer cells vs normal cells; i.e., EGCG-mediated inhibition of NF-kappaB constitutive expression and activation was found to occur at much higher dose of EGCG in NHEK as compared to A431 cells. This study suggests that EGCG-caused cell cycle deregulation and apoptosis of cancer cells may be mediated through NF-kappaB inhibition.

Apoptosis↗

Growth inhibition, cell-cycle dysregulation, and induction of apoptosis by green tea constituent (-)-epigallocatechin-3-gallate in androgen-sensitive and androgen-insensitive human prostate carcinoma cells.

Prostate cancer (PCA) is the most prevalent cancer diagnosed and the second leading cause of cancer-related deaths among men in the United States. Descriptive epidemiological data suggest that androgens and environmental exposures play a key role in prostatic carcinogenesis. Since androgen action is intimately associated with proliferation and differentiation, at the time of clinical diagnosis in humans most PCA represent themselves as a mixture of androgen-sensitive and androgen-insensitive cells. Androgen-sensitive cells undergo rapid apoptosis upon androgen withdrawal. On the other hand, the androgen-insensitive cells do not undergo apoptosis upon androgen blocking, but maintain the molecular machinery of apoptosis. Thus, agents capable of inhibiting growth and/or inducing apoptosis in both androgen-sensitive and androgen-insensitive cells will be useful for the management of PCA. In the present study, we show that (-)-epigallocatechin-3-gallate (EGCG), the major polyphenolic constituent present in green tea, imparts antiproliferative effects against both androgen-sensitive and androgen-insensitive human PCA cells, and this effect is mediated by deregulation in cell cycle and induction of apoptosis. EGCG treatment was found to result in a dose-dependent inhibition of cell growth in both androgen-insensitive DU145 and androgen-sensitive LNCaP cells. In both the cell types, EGCG treatment also resulted in a dose-dependent G(0)/G(1)-phase arrest of the cell cycle as observed by DNA cell-cycle analysis. As evident by DNA ladder assay, confocal microscopy, and flow cytometry, the treatment of both DU145 and LNCaP cells with EGCG resulted in a dose-dependent apoptosis. Western blot analysis revealed that EGCG treatment resulted in (i) a dose-dependent increase of p53 in LNCaP cells (carrying wild-type p53), but not in DU145 cells (carrying mutant p53), and (ii) induction of cyclin kinase inhibitor WAF1/p21 in both cell types. These results suggest that EGCG negatively modulates PCA cell growth, by affecting mitogenesis as well as inducing apoptosis, in cell-type-specific manner which may be mediated by WAF1/p21-caused G(0)/G(1)-phase cell-cycle arrest, irrespective of the androgen association or p53 status of the cells.

Androgens↗

Ultrasonography of spontaneous lesions of the genital system of three rams, and their influence on semen quality.

Three young Suffolk ram lambs had lesions which rendered them reproductively unsound. One had a unilateral scrotal hernia, detected by palpation, and two had sperm granulomas which were detected by trans-scrotal ultrasonography at 18 to 20 weeks of age, before they could be detected by palpation. Changes in the lesions were monitored ultrasonographically at two-week intervals with a 7.5 MHz linear array transducer. On the day of each examination, semen was collected from the rams with sperm granulomas by using an artificial vagina, and their libido was assessed. Semen could rarely be collected from the third ram. Comparisons were made with similar data obtained from two normal rams. When the rams were 20 to 21 months of age, they were vasectomised on the normal side, so that the influence of the lesions on semen composition and libido could be assessed, and semen was collected and evaluated until they were euthanised at approximately 24 months of age, when the genital system was examined for gross lesions. The sperm granulomas changed in size (one of them increased in size by about 30 times) and echotexture over the 19-month period of the study, whereas the scrotal hernia, which contained omental fat, remained fairly constant. The libido of the two rams with sperm granulomas was comparable with the two normal controls. The total mean (sem) number of sperm in the ejaculates were 1.11 (0.10) x 10(9) and 2.03 (0.17) x 10(9) sperm/ml in the affected rams and 4.11 x 10(9) sperm/ml in the normal rams over the same period; the differences were significant (P<0.05). After unilateral vasectomy, the ejaculates from these two rams contained small numbers of dead spermatozoa, mostly with degenerate heads. Postmortem examination confirmed the gross lesions identified ultrasonographically.

Animals↗

Green tea and skin.

OBJECTIVE: To discuss the current knowledge of polyphenolic compounds present in green tea as anti-inflammatory, antioxidant, and anticarcinogenic in skin. DATA SOURCES: References identified from bibliographies of pertinent articles, including our work in related fields. STUDY SELECTION AND DATA EXTRACTION: Articles were selected based on the use of green tea or its polyphenolic constituents for prevention against inflammation and cancer in the skin. Also discussed is the possible use of green tea to treat various inflammatory dermatoses. DATA SYNTHESIS: The polyphenolic compounds from green tea were tested against chemical carcinogenesis and photocarcinogenesis in murine skin. These green tea polyphenols were found to afford protection against chemical carcinogenesis as well as photocarcinogenesis in mouse skin. A few experimental studies were conducted in human skin in our laboratory. Analysis of published studies demonstrates that green tea polyphenols have anti-inflammatory and anticarcinogenic properties. These effects appear to correlate with antioxidant properties of green tea polyphenols. CONCLUSIONS: The outcome of the several experimental studies suggests that green tea possess anti-inflammatory and anticarcinogenic potential, which can be exploited against a variety of skin disorders. Although more clinical studies are needed, supplementation of skin care products with green tea may have a profound impact on various skin disorders in the years to come. Arch Dermatol. 2000;136:989-994

Administration, Oral↗

Over-expression of cyclooxygenase-2 in human prostate adenocarcinoma.

Aberrant or increased expression of cyclooxygenase (COX)-2 has been implicated in the pathogenesis of many diseases including carcinogenesis. COX-2 has been shown to be over-expressed in some human cancers. Employing semi-quantitative reverse transcription-PCR, immunoblotting, and immunohistochemistry we assessed COX-2 expression in samples of pair-matched benign and cancer tissue obtained from the same prostate cancer patient. Mean levels of COX-2 mRNA were 3.4-fold higher in prostate cancer tissue (n = 12) compared with the paired benign tissue. The immunoblot analysis demonstrated that as compared to benign tissue COX-2 protein was over-expressed in 10 of 12 samples examined. Immunohistochemical analysis also verified COX-2 over-expression in cancer than in benign tissue. To our knowledge, this is the first in vivo study showing an over-expression of COX-2 in prostate cancer. These data suggest that COX-2 inhibitors may be useful for prevention or therapy of prostate cancer in humans.

Adenocarcinoma↗

Patterning of olfactory sensory connections is mediated by extracellular matrix proteins in the nerve layer of the olfactory bulb.

In early rat embryos when axons from sensory neurons first contact the olfactory bulb primordium, lactosamine-containing glycans (LCG) are detected on neurons that are broadly distributed within the olfactory epithelium, but that project axons to a very restricted region of the ventromedial olfactory bulb. LCG(+) axons extend through channels defined by the coexpression of galectin-1 and beta2-laminin. These two extracellular matrix molecules are differentially expressed, along with semaphorin 3A, by subsets of ensheathing cells in the ventral nerve layer of the olfactory bulb. The overlapping expression of these molecules creates an axon-sorting domain that is capable of promoting and repelling subsets of olfactory axons. Specifically, LCG(+) axons preferentially grow into the region of the nerve layer that expresses high amounts of galectin-1, beta2-laminin, and semaphorin 3A, whereas neuropilin-1(+) axons grow in a complementary pattern, avoiding the ventral nerve layer and projecting medially and laterally. These studies suggest that initial patterning of olfactory epithelium to olfactory bulb connections is, in part, dependent on extracellular components of the embryonic nerve layer that mediate convergence and divergence of specific axon subsets.

Age Factors↗

Involvement of nitric oxide in nickel-induced hyperglycemia in rats.

Nitric oxide is an important bioactive signaling molecule that mediates a variety of normal physiological functions which, if altered, could contribute to the genesis of many pathological conditions, including diabetes. In the present study we have shown the involvement of NO in nickel-induced hyperglycemia in male albino rats. Administration of nickel chloride (25 to 100 micromol/kg; ip) to overnight-fasted rats resulted in significant dose and time-dependent increase in plasma glucose, attaining maximum level at 1 h posttreatment and thereafter decreasing to normal levels by 4 h. The involvement of NO in nickel-induced hyperglycemia was evident by the observation that pretreatment of rats with NG-monomethyl-l-arginine (10 to 50 micromol/kg; ip), an inhibitor of nitric oxide synthase (NOS), significantly attenuated the nickel-mediated increase in the plasma glucose levels in a dose-dependent fashion. The activity of Ca(2+)-dependent NOS (constitutive form, c-NOS) was found to be significantly elevated in adrenals (5.5-fold) and brain (1.4-fold) at 1 and 2 h posttreatment, attaining normal levels by 4 h. In contrast, the activity of c-NOS in pancreas was significantly decreased (2.8-fold) with a concomitant increase (11.6-fold) in inducible NOS (i-NOS) at the same time interval. As observed by immunoblot analysis, a significant increase in i-NOS protein expression in the pancreas was observed at 1 and 2 h posttreatment. This was associated with a significant elevation in cGMP levels in adrenals, brain, and pancreas, possibly via the stimulation of cytosolic guanylate cyclase. This elevation in cGMP was abolished by low concentration of hemoglobin. These effects were associated with the accumulation of nickel in the target tissues. Taken together, our data suggest that nickel causes a significant increase in the levels of (i) cGMP and c-NOS in adrenals and brain and (ii) i-NOS in pancreas. These events may be responsible for modulating the release of insulin from pancreas finally leading to hyperglycemic condition in rats.

Adrenal Glands↗

Suppression of oxytocin-induced prostaglandin F2alpha release after intra-uterine nordihydroguariaretic acid administration in ewes.

Intrauterine administration of the 5-lipoxygenase inhibitor nordihydroguariaretic acid (NDGA; 5 mg, bid) on Days 9-14 of the ovine estrous cycle (estrus = Day 0) delayed luteolysis and extended the duration of the estrous cycle (20+/-1, SD, vs. 16+/-1 days; P < 0.01). In control ewes, plasma concentrations of 13,14,dihydro-15-keto prostaglandin F2alpha increased significantly (P < 0.001) following i.v. administration of oxytocin (10 i.u.) on Day 14; in the nordihydroguariaretic acid-treated ewes, however, there was no such increase. In addition, concentrations of endometrial oxytocin receptors were significantly less (P < 0.01) in the nordihydroguariaretic acid-treated ewes (218+/-60 vs. 579+/-66 fmol/mg tissue). These results suggest that 5-lipoxygenase products of arachidonate metabolism may be involved in the control of ovine luteal function.

Animals↗

Mechanism of biochemical action of substituted 4-methylbenzopyran-2-ones. Part 7: Assay and characterization of 7,8-diacetoxy-4-methylcoumarin:protein transacetylase from rat liver microsomes based on the irreversible inhibition of cytosolic glutathione S-transferase.

The enzymatic transfer of acetyl groups from acetylated xenobiotics to specific proteins is a relatively grey area in the evergreen field of biotransformation of foreign compounds. In this paper, we have documented evidence for the existence of a transacetylase in liver microsomes that catalyses the transfer of acetyl groups from 7,8-diacetoxy-4-methylcoumarin (DAMC) to glutathione S-transferase (GST), either purified or present in cytosol leading to the irreversible inhibition of GST. A simple procedure is described for the assay of transacetylase by preincubation of DAMC with liver microsomes and pure GST/liver cytosol, followed by the addition of 1-chloro-2,4-dinitrobenzene (CDNB) and reduced glutathione (GSH) in order to quantify GST activity by the conventional procedure. The extent of inhibition of GST by DAMC under the conditions of the assay is indicative of DAMC:protein transacetylase activity. Following the assay procedure described here, the transacetylase was shown to exhibit hyperbolic kinetics. The bimolecular nature of the transacetylase reaction was apparent by the demonstration of Km and vmax values. 7,8-Dihydroxy-4-methylcoumarin (DHMC), one of the products of transacetylase reaction was identified and quantified using the partially purified enzyme. The fact that p-hydroxymercuribenzoate (PHMB) and iodoacetamide abolished irreversible inhibition of GST upon the action of transacetylase on DAMC strongly characterized transacetylase as a protein containing thiol group at the active site. In addition, the relative specificities of acetoxy 4-methylcoumarins to transacetylase have been demonstrated.

Acetylation↗

Involvement of Fas (APO-1/CD-95) during photodynamic-therapy-mediated apoptosis in human epidermoid carcinoma A431 cells.

Photodynamic therapy is a promising treatment modality for a variety of cutaneous neoplasms and other skin disorders. Studies suggest an involvement of multiple pathways during photodynamic-therapy-mediated cell death. A complete knowledge of the mechanisms involved in photodynamic therapy may lead to an improvement in its therapeutic efficacy. In vitro as well as in vivo studies have shown the involvement of apoptosis during photodynamic- therapy-mediated cell death. The pathways by which photodynamic therapy causes this are not fully understood. In this study, employing human epidermoid carcinoma (A431) cells and silicon phthalocyanine 4 photodynamic therapy, we show that the cell surface death receptor Fas (also known as APO-1 or CD-95) pathway is an important contributor to photodynamic-therapy-mediated apoptosis. Employ- ing flow cytometric analysis and confocal microscopy we first established that silicon phthalocyanine 4 photodynamic therapy results in a significant induction of apoptosis in A431 cells. Immunoblot analysis revealed a significant time-dependent increase in the protein expression of Fas at 5, 15, 30, and 60 min post-photodynamic therapy followed by a decrease at later time-points (2 and 3 h post-photodynamic therapy). A Fas enzyme-linked immunosorbent assay demonstrated an increase in this protein in cell culture medium starting at 1 h post-photodynamic therapy and showing a time-dependent response up to 3 h following therapy, suggesting a diffusion of soluble Fas from cells into the medium from 1 h after photodynamic therapy. Silicon phthalocyanine 4 photodynamic therapy also resulted in a time-dependent increase in (i) the multimerization of Fas protein, (ii) the protein expression of Fas ligand, (iii) FADD, an adapter molecule for Fas, and (iv) the binding of FADD with Fas. Silicon phthalocyanine 4 photodynamic therapy also caused a significant activation of FLICE, as evident from the appearance of cleaved products of pro-caspase 8. Further, a pretreatment of cells with rhFas:Fc fusion protein or general caspase inhibitor Z-VAD-FMK followed by silicon phthalocyanine 4 photodynamic therapy resulted in a significantly enhanced cell survival. Taken together, our data, for the first time, delineate an involvement of the Fas pathway as an important contributor to photodynamic-therapy-mediated apoptosis of cancer cells. These observations may be important for improving the efficacy of photodynamic therapy for the treatment of skin cancer and possibly other skin disorders. J Invest Dermatol 115:1041-1046 2000

Apoptosis↗

Assessment of the levels of chlorinated pesticides in breast milk in Kuwait.

Breast milk samples, randomly collected from 32 Kuwaiti donors were analysed for chlorinated pesticides. DDE residues ranged from 127 to 3333 micrograms/kg, averaging, 833 micrograms/kg, expressed on a fat weight basis. DDT levels ranged from 0.6 to 67 micrograms/kg fat and averaged 12.4 micrograms/kg, fat. High DDE/DDT ratios were found, which indicated that the exposure to DDT, in most cases, happened quite some time ago. In addition many of the samples also contained isomers of HCH, heptachlor-epoxide, aldrin, dieldrin and endrin. Residue levels of non-DDT pesticides were generally low. Overall levels of DDT-pesticides in Kuwaiti milk samples were lower than levels reported from other Middle Eastern countries, although methodologies may not be directly comparable.

Environmental Exposure↗